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Basic nerve conduction study

By
Mohammad Hassan Abu-Zaid
Ass. lect. of
Rheumatology & Rehabilitation
MOTOR CONDUCTION
STUDIES
• The CMAP is a biphasic potential with an
initial negativity, or upward deflection from the
baseline
• For each stimulation site:the latency,
amplitude, duration, and area of the CMAP
are measured .
• A motor conduction velocity can be calculated
after two sites of stimulation, one distal and one
proximal.
• It’s called M response
CMAP
• If an initial positive deflection exists, it
may be due to:
1. Inappropriate placement of the active
electrode from the motor point
2. Volume conduction from other muscles
or nerves
3. Anomalous innervations
CMAP electrode placement.
I: Over the endplate region.
II: Off the endplate region.
• The active recording electrode is placed
on the center of the muscle belly (over the
motor endplate), and the reference
electrode is placed distally about 3:4 cm
• The stimulator then is placed over the
nerve that supplies the muscle, with the
cathode placed closest to the recording
electrode.
• As current is slowly increased from a
baseline: more of the underlying nerve
fibers are brought to action potential, and
subsequently more muscle fiber action
potentials are generated.
• most nerves require a current in the range
from 20 to 50 mA to achieve supramaximal
stimulation.
• The recorded potential, known as the compound
muscle action potential (CMAP), represents the
summation of all underlying individual muscle
fiber action potentials.
• When the current is increased to the point that the
CMAP no longer increases in size, one presumes
that all nerve fibers have been excited and that
supramaximal stimulation has been achieved. The
current then is increased by another 20% to ensure
supramaximal stimulation.
Latency
• Latency measurements usually are made
in milliseconds (ms).
• The latency is the time from the stimulus
to the initial negative deflection from
baseline
• In CMAP latency represents three
separate processes:
(1) the nerve conduction time .
(2) the time delay across the NMJ
(3) the depolarization time across the
muscle.
• The only major difference between
CMAPs produced by proximal and distal
stimulations is the latency.
Conduction Velocity
• It’s measurement of the speed of the
fastest conducting nerve axons
• It is calculated by dividing the change in
distance (between proximal stimulation
site & distal stimulation site in mm) by
the change in time (proximal latency in
msec minus distal latency in ms)
Conduction Velocity
• Normal values are > 50 meters/sec in
the upper limbs
And > 40 meters/sec in the lower limbs.
Amplitude
• it is most commonly measured from
baseline to the negative peak (baseline-to-
peak) and less commonly from the first
negative peak to the next positive peak
(peak-to-peak).
• CMAP amplitude reflects the number of
muscle fibers that depolarize.
Although low CMAP amplitudes most often
result from loss of axons (as in a typical
axonal neuropathy), other cause of a low
CMAP amplitude include conduction block
from demyelination located between the
stimulation site and recorded muscle
• average CMAP amplitude 3 mv
Duration
• This is measured from the initial deflection
from baseline to the final return, also is
measured from the initial deflection from
baseline to the first baseline crossing& it’is
preferred as a measure of CMAP duration
because when CMAP duration is measured
from the initial to terminal deflection back
to baseline, the terminal CMAP returns to
baseline very slowly and can be difficult to
mark precisely.
• It depends on the summation and rate
of firing of numerous axons.
• Duration characteristically increases in
conditions that result in slowing of
some motor fibers (e.g., in a
demyelinating lesion).
• average CMAP duration 14: 16.5 msec
Area
• This is a function of both the amplitude and
duration of the waveform.
• CMAP area is measured between the baseline and
the negative peak.
• Differences in CMAP area between distal and
proximal stimulation sites are significant in the
determination of conduction block from a
demyelinating lesion
SENSORY CONDUCTION
STUDIES
• A pair of recording electrodes (GI and G2)
are placed in line over the nerve at an
interelectrode distance of 3 to 4 cm, with
the active electrode (G I) placed closest to
the stimulator.
• Recording ring electrodes are
conventionally used to test the sensory
nerves in the fingers
• A sensory nerve study represents the
conduction of an impulse along the sensory
nerve fibers
• The SNAP usually is biphasic or triphasic in
configuration with initial negative
deflection .
• sensory fibers usually have a lower
threshold to stimulation than do motor
fibers
SNAP CMAP
Latency
• Onset latency is the time required for an
electrical stimulus to initiate an evoked
potential.

• onset latencies reflect conduction along the


fastest nerve fibers
• Peak latency in SNAP : it represents the
latency along the majority of the axons and
is measured at the peak of the waveform
amplitude (first negative peak).
• Both latencies are primarily dependent on
the myelination of a nerve.
Advantages of peak latency
measurements in SNAPs
• The peak latency can be ascertained in a
straightforward manner. some potentials,
especially small ones, it may be difficult to
determine the precise point of deflection
from baseline
• N.B peak latency cannot be used to
calculate a conduction velocity
Amplitude
• The SNAP amplitude reflects the sum of
all the individual sensory fibers that
depolarize.
• Low SNAP amplitudes indicate a definite
disorder of peripheral nerve.
Duration
• Similar to the CMAP duration
Conduction Velocity
• Only one stimulation site is required to
calculate a sensory conduction velocity.
SNAP & localizing lesion

• It can also be useful in localizing a lesion


in relation to the dorsal root ganglion
(DRG).
• The DRG is located in the intervertebral
foramen and contains the sensory cell
body.
• Lesions proximal to it
(injuries to the sensory
nerve root or to the
spinal cord) preserve
the SNAP waveform
despite clinical sensory
Abnormalities
• This is because axonal
transport from the
DRG to the peripheral
axon continues to
remain intact.
Technical Considerations
• Antidromic and Orthodromic Recording
• Antidromic studies are easier to record a
response than orthodromic studies.
• May be more comfortable than orthodromic
studies due to less stimulation required.
• May have larger amplitudes due to the
nerve being more superficial at the distal
recording sites.
1.Antidromic stim.
2.orthdromic stim of same n
Temporal dispersion and phase
cancellation
• (SNAPs) and(CMAPs) both are compound
potentials, representing the summation of
individual sensory and muscle fiber action
potentials, respectively.
• In each case, there are fibers that conduct faster
and those that conduct more slowly
• With distal stimulation, fast and slow fiber
potentials arrive at the recording site at
approximately the same time
• With proximal stimulation, the slower fibers lag
behind the faster fibers.
Temporal Dispersion
• This reflects the range of conduction
velocities of the fastest and slowest nerve
fibers.
• It is seen as a spreading out of the
waveform with proximal compared to distal
stimulation.
Phase Cancellation
• When comparing a proximal to distal stimulation,
a drop in amplitude and increase in duration
occurs, mostly with a (SNAP) because of its short
duration.
• When the nerve is stimulated, the action potentials
of one axon may be out of phase with neighboring
ones. The negative deflections of one axon can
then cancel the positive deflection of another,
reducing the amplitude.
• The summation of these axons creates an action
potential that appears as one long prolonged wave.
• For this reason a drop of 50% is considered
normal when recording a proximal SNAP.

• Drop of 15% is considered normal when


recording a proximal CMAP
Patterns of nerve conduction
Normal study of median nerve.

• Note the normal


median distal latency
(DL) 3 ms, amplitude
>4 m V, and
conduction velocity
(CV) >49 mls.
Axonal loss.

• amplitudes decrease
• CV is normal or slightly
slowed.
• DL is normal or slightly
prolonged.
• The morphology of the
potential does not change
between proximal and
distal sites.
Demyelination
associated with inherited
conditions (uniform)
• CV is markedly slowed <
75% lower limit of
normal)
• DL is markedly
prolonged (>130% upper
limit of normal).
• However, there usually is
no change in
configuration between
proximal and distal
stimulation
Demyelination with conduction
block usually acquired as GBS
• Marked slowing of
conduction velocity
and distal latency, but
also with change in
potential morphology
(conduction
block/temporal
dispersion) between
distal and proximal
stimulation sites,
CMAP amplitude and conduction
block location.

Late responses may be abnonl


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• In both patients, there is a drop in amplitude
across the spiral groove

• In patient 1, block. Conduction block signifies


demyelination; therefore, the prognosis is good.

• In patient 2, This implies significant axonal loss.


Although there is some conduction block across
the spiral groove & most of patient's weakness is
secondary to axonal loss, which implies a longer
and possibly less complete recovery process.
Late Responses
1. F wave
2. H reflex
3. A wave
F wave

• Stimulation is followed by depolarization which travels


in both directions: first directly to the muscle fiber
producing the M response, and retrograde up to the
motor axon and to the neuron, where it is re propogated
back through the axons to produce the delayed F
response.
• The F-wave is a small late motor response
occurring after the CMAP.
• It represents a late response from
approximately 1–5% of the CMAP
amplitude.
• It is produced using supramaximal
stimulation
• The F-wave is a pure motor response and
does not represent a true reflex because
there is no synapse along the nerve pathway
being stimulated
• The configuration and latency change with
each stimulation due to activation of
different group of anterior horn cells with
each stimulation
• Configuration :Usually polyphasic& varies
with each stimulation
• Amplitude 1%-5% CMAP
• Measurements: Minimal, maximal latency
Chronodispersion and Persistence
• Chronodispersion: it’s the time delay bet.
Minimal& maximal latencies
• Normal values
• <32 ms median/ulnar· stim. at wrist
• <56 ms peroneal/tibial· stim. at ankle
• Compare symptomatic to asymptomatic
side
• Chronodispersion <4 ms (median/ulnar)
&<6 ms (peroneal/tibial)
• Persistence >50%
N.B
• Normally 1- peroneal F waves may be
absent or nonpersistent
2-F responses may be absent in
sleeping or sedated patients
• F responses may be absent with low-
amplitude distal CMAPs
Significance of F wave
• Early stage of mild P.N
• Demonstrating isolated proximal lesions as
early AIDP (GBS)
• Plexopathy

F wave & radiculopathy
• F-waves are insensitive in detecting radiculopathy due to:
1. The recorded muscle usually is innervated by more than
one root. Thus in single level radiculopathy, normal
conduction through uninvolved root results in normal F-
wave latency despite of compressed neighboring root.
2. However root compression, there's normal F-wave
because the surviving axons are conducting normally.
3. If focal slowing occurs at the root segment of the motor
axon, delay in F-wave latency becomes diluted by the
relatively long motor axon & to avoid that dilution
4. In U L commonly used are F median & ulnar ns which
demonstrates C8& T1 roots ( uncommon sites of
radiculopathy)
F wave latency & central
conduction
• proximal conduction may be detected by
equation (F proximal - M proximal - 1ms)/2.
Also detection of F/M ratio by equation (F
proximal-M proximal-1ms)/ (2M proximal).
Normal=0.8:0.9 if increased, so proximal
lesion and vice versa.
Axillary F-loop latency
• AFLL= F-wave wrist +distal motor latency -
2(axillary motor latency). Normal values for
median & ulnar nerves were reborted as
14:16ms
F - estimate
• F estimate = (2D/CV) x 10 + 1 ms + DL
H reflex

• It’s obtained by submaximal stimulation of the afferent


sensory fiber resulting in orthodromic conduction to the
spinal cord. In the spinal cord, there is synaptic
stimulation of the alpha motor neuron, this results in the
evoked H response in the muscle.
• A rudimentary M response is produced when a few motor
axons are directly stimulated.
• Formula :
H-reflex = 9.14 + 0.46 (Leg length in cm from
the medial malleolus to the popliteal fossa)
+ 0.1 (age)
• Latency
Normal: 28–30 milliseconds
Side to side difference: greater than 0.5–1.0
ms is significant
Above 60 years: adds 1.8 milliseconds
• Location
• Soleus muscle: tibial nerve: S1 pathway
• Flexor carpi radialis: median nerve: C7
pathway
• Vastus medialis : femoral n : L4 pathway
A-(AXON) WAVE
• The axon reflex (A wave), although not a true
reflex, it is another late potential that often is
recognized during the recording of F responses.
The axon reflex typically occurs between the F
response and the direct motor (M) response
• An axon reflex is identified as a small motor
potential that is identical in latency and
configuration with each successive stimulation.
• Axon reflexes typically are seen in
reinnervated nerves, especially when a
submaximal stimulus is given
• Function
This waveform represents collateral sprouting
following nerve damage.
Normal. Submax. Supramax.
BLINK REFLEX
• It is an electrically evoked analogue to the corneal
reflex.
• It is initiated by stimulating the supraorbital
branch of the trigeminal nerve.
• The response propagates into the pons and
branches to the lateral medulla.
• It then branches to innervate the ipsilateral and
contralateral orbicularis oculi via the facial nerve.
Blink reflex anatomy
• The afferent loop of the blink reflex is
mediated by the first division of the
trigeminal nerve
• synapses with both the main sensory
nucleus of cranial nerve V in the midpons
and the nucleus of the spinal tract of cranial
nerve V in the medulla.
• The efferent pathway is mediated via
bilateral facial nerves to the orbicularis
oculi muscles.
• Two responses are evaluated, an ipsilateral R1 and
bilateral R2.
• R1 potential is mediated by a disynaptic
connection between the main sensory nucleus and
the ipsilateral facial motor nucleus (VII).
• R2 responses are mediated by a multisynaptic
pathway between the nucleus of the spinal tract of
cranial nerve V and both ipsilateral and
contralateral facial nuclei (VII).
Normal Latency
• R1 < 13 milliseconds
• R2 Ipsilateral (direct) < 40 milliseconds
• R2 Contralateral (consensual) < 41
milliseconds

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