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EMG Summary

Basic Concepts
1. NCS = Nerve-conduction study
a. Types of NCS:
i. Sensory: Stimulating the nerve, recording from the innervated skin
ii. Motor: Stimulating the nerve, recording from the muscle
b. Can be performed on any accessible nerve
c. Output parameters:
i. How fast the impulse travels
ii. Action potential morphology
d. Study Terms
i. Action Potential:
1. Compound Nerve Action Potential = CNAPs (for mixed
nerves)
2. Compund Motor Action Potential = CMAP
3. Sensory Nerve Action Potential = SNAP
ii. Latency: time-interval between onset of stimulus and onset of
response
1. Motor latency
2. Sensory latency
iii. Amplitude: maximal height of action potential
iv. F-wave: a CMAP evoked antidromically (recorded at the
muscle) after stimulating motor-nerve maximally. Represents
the time needed for a stimulus to travel antidromically
towards the spinal cord and return orthodromically to the
muscle along a very small percentage of the fibers
v. H-wave: a CMAP evoked by orthodromically stimulating
sensory fibers, synapsing at the spinal level and returning
orthodromically via motor fibers. Thought to represent
monosynaptic spinal refelex – Hoffman reflex (found in adults
in the gastro-soleus and FCR).
2. EMG= Electromygraphy:
a. Only the muscle is tested, nerves are tested indirectly
b. There is no stimulation, spontaneous muscle electrical activity is
recording during rest and contraction

Stations tested in elecro-diagnostic studies:


CMAP
Anti
Ortho

F-Wave Motor Nerve


Muscle Peripheral Nerve MN
Spinal Cord
Sensory Nerve H-Wave
SNAP
DRG

Technical Aspects
1. Electrodes
a. NCS:
i. Active/Pickup – surface
ii. Reference – surface
iii. Ground – surface
b. EMG
i. Active – needle
ii. Reference- surface (if active is monopolar)
iii. Ground – surface
2. Amplification & Filtration:
a. common-mode rejection: a techinique to eliminate common
exogenous electrical artifacts (machinery, ECG, remote muscles
potentials)
b. High-pass filters: filters low-frequency signals that if present cause a
wandering baseline (for motor NCS: 10Hz, sensory NCS: 2-10 Hz)
c. Low-pass: filters high-frequency signals that if present can obscure
small signals (such as SNAPs, fibbrillations) and cause noisy baseline.
(for motor NCS: 10 KHz, sensory NCS: 2 KHz)
3. Sources of Error:
a. Stimulus artifact. Make sure that the ground is between the recording
and stimulating electrodes to minimize it.
b. Reaching to the Supra-maximal point – the point in which increasing
the stimulus strength won't produce an amplitude increment. Failure
to detect the point mioght lead to misdiagnosis of axonal damage
(distal) or conduction block (proximal). Increasing stimulation above
the supra-maximal point might lead to stimulation of nerves far from
the nerve of interest
c. Measurement errors. Must follow the nerve.
4. Stimulators:
a. Cathode (black / negative pole) is placed towards the direction in
which the nerve is to be stimulated.

Nerve Conduction Studies


1. Physiology if Nerve Conduction
a. Done only on myelinated fibers. Unmyelinated fibers are extremely
slow and do not contribute significantly to CMAPs and SNAPs
b. Myelinated nerve transfer signal in a saltatory way in velocity of 40-
70 m/sec
c. Unmyelinated nerve transfer signal in a continuous way in velocity of
1-5 m/sec. This velocity is largely dependent on the opening speed of
volume dependent sodium channels.
d. De-myelinated nerve may not be able to conduct a signal along the
de-myelinated site – "Conduction Block", neuropraxia. Ususally, up to
20% decrement of amplitude
e. Re-myelination produce an
immature myelin in the first stage.
faster slower
This myelin is less insulating than
mature myelin, thus the velocity will
be decreased.
2. The Action Potential:
a. Types:
i. CMAP = summation of motor
units potentials
ii. SNAP = summation of
sensory nerve fibers
b. AP Components:
i. Area = area under the
upward deflection ("negative")
ii.
iii. Latency = the time from stimulation to action potential onset
1. In sensory nerves, dependent on:
a. conduction velocity of the fastest fibers
b. the distance the wave of depolarization travels
2. In motor nerves, dependent
a. conduction velocity of the fastest fibers
b. the distance the wave of depolarization travels
c. synaptic transfer time
Typically approximately 1 d. intra-muscular conduction speed
msec

3. Measuring Conduction Velocity


a. For sensory nerves: v = distance / time
b. For motor nerves = v = delta-distance / delta-
time (due to conduction via the NMJ and the
muscle). Require stimulation at two sites.
c. Normal CVs: >50 m/s (upper limb); >40 m/s
(lower limb)
iv. Amplitude - could be measured from onset to peak or from
peak to trough
1. CMAPs amplitude represents the sum of amplitudes of
individual muscle fibers that are depolarized by a
single motor fiber of certain conduction velocity.
2. Dependent on:
a. Integrity of axons
b. Integrity of muscle fibers
c. Extent of variability of conduction velocity of
individual fibers (i.e., if some fibers are slow and
others are fast, then the AP will be of longer
duration and lower amplitude)  low
amplitude + greater duration = some fibers are
slowly conducting
v. Duration = time from onset to recovery
1. Duration is increased in acquired as opposed to
congenital neuropathies
3. Stimulation must be done as close to the nerve as possible (anatomy).
4. Recording:
a. Active Electrode (E1 or G1):
i. Motor: placed on the muscle belly, preferably on the motor
point, where the nerve enters the muscle
ii. Sensory: over the nerve, where the nerve is superficial as
possible
b. Reference Electrode (E2 or G2):
i. CMAP: placed on a nearby tendon or bone away from the
muscle
ii. SNAP: place 3-4 cms orthodromically
c. Ground Electrode: placed between the stimulating electrode and the
recording electrode.
5. Late Responses
Spinal a. H-Reflex:
cord i.Conduction
Mono- or oligo-synaptic
of electrical stimulusspinal reflex involving both motor and
orthodromically along the
sensory fibers tibial nerve (sensory)
ii. Corresponds to deep tendon reflexes, and usually when they
are present, it is also present
iii. Sensitive measure for radiculopathy, because:
1. Helps to assess proximal lesions
2. Becomes abnormal relatively early in the development
of radiculopathy
3. Activated by sensory fiber which is proximal to the DRG
iv. S1 Radiculopathy:
1. Record H-Reflex latency from gastrocnemius-soleus
upon stimulating tibial nerve in the popliteal fossa,
of H-wave
moving
ortho-
dormically
along the
tibial nerve
(motor)
cathode proximal to anode, with submaximal
stimulation
2. When stimulation intensity: H-wave decrease and M-
wave increase. With supra-maximal stimulation, H-
reflex is usually absent
3. S1 radiculopathy is diagnosed when side-to-side
latency differences are >1.5 msec or side-to-side
amplitude difference of >60%
4. Useful to differentiate S1 radiculopathy from L5-
radiculopathy
5. Limitations  sensitive but not specific
a. Could be normal in patients with S1-
radiculopathy
b. Abnormal H-reflex is only suggestive but not
definitive, because abnormality might originate
from other components of the pathway
(peripheral nerves, plexus, spinal cord)
c. Once H-reflex becomes abnormal, it doesn't
return to normal
d. H-reflex is often absent in otherwise normal
individuals aged >60 yrs
v. C6/7 Radiculopathy
1. Less performed in clinical settings
2. Recording over FCR; Stimulating over the median nerve
at the elbow
vi. Guillian-Barre syndorme
b. F-wave:
i. Low amplitude responses to be due antidromic activation of
motor neurons, which then pass orthodromic impulses back
along motor axons.
ii. Discovered first in intrinsic foot muscles (so called "foot
wave")
iii. Amplitude low (5% of M-response), Vairable configuration,
variable latency
iv. Most commonly used parameter is the latency of the shortest
reproducible response.
v. F-waves are not sensitive test because:
1. Pathway involves only motor fibers
2. The pathway is long, lesions could be obscured: any
lesion between the muscle being tested and the
anterior horn cell could affect the F-wave similarly
3. Muscles are innervated by multiple roots, F-wave could
originate from healthy fibers in the non-affected root
4. Latencies are variables, so multiple stimulations should
be made, more than 10.
vi. Side-to-side difference indicating a pathology
1. Hand: >2 msec
2. Calf: >3 msec
3. Foot: >4 msec
vii. Equation, used in order not to measure distances for F-wave:
F-wae Ratio = (F-M-1)/2M, where M is the CMAP latenct and F
is the F-wave latency.
1. F-wave ratio > 1.3 indicates a proximal lesion
2. F-wave ratio <0.7 indicates distal lesion
3. Interpreting F-wave ratio is not more accurete than F-
wave latencies, and should be done in conjunction with
other data
viii. F-waves could be elicited in most muscles, but distal muscles
are preferred
ix. Stimulation site is along the peripheral nerve, the cathode
should be proximal
x. Other uses:
1. Demyelinating polyneuropathies
2. Guillian-Barre
3. Proximal nerve or root injury
c. General Recommendations
i. When stimulating the same nerve at a proximal and distal
points, the morphology and the duration should be similar,
and distal amplitude should be decrease more than 20%,
compared to the proximal amplitude.
ii. Non-identical waveforms may be due to stimulation of other
nerves (e.g., tibial and peroneal, which lie close in the popliteal
fossa)
iii. The greater the distance between stimulation points for motor
nerves, the smaller impact will be for length measurement
error.
iv. Conduction block (segmental demyelination on the segment
being stimulated) could be diagnosed by either:
1. Increase in duration with smaller amplitude on
proximal stimulation + AUC of CMAP doesn’t change
OR
2. Decrease of more than 20% amplitude with the
proximal stimulation (compared to the distal
amplitude)
v. Estimation of amount of axonal damage could be done when
one side is affected by comparing the CMAP amplitude of the
affected to the unaffected side. It is linearly correlated.
vi. When stimulating the ulnar nerve, elbows should be bent to
70-90 degrees. Elbow which is held straight causes the
calculation of conduction velocity to be falsely decreased.
Elbows should be in the same position for side-to-side
comparison.

Electromyography
1. Muscle Physiology
a. Membrane potential of muscle fibers is -80 mV
b. EMG is measuring of the electrical excitation of the myofibers
c. Motor unit =
i. One anterior horn cell
ii. Its axon
iii. The muscle fiber innervated by the axon
d. Recruitment of motor units is done from the smallest (level I) if lowest
threshold to the largest with higher threshold
2. Technical Aspects
a. Electrodes
i. Needle Electrodes

Monopolar Concentric
Other electrodes Reference, Ground Ground
requirements
Radius of 360 180
Recording
Sensitivity More sensitive, useful for Higher signal-to-
polyphasicity, but more noisy noise ratio
Diameter Smaller Larger
Pain Less More
Cost Less More

3. Components of the measurement:


a. Insertional activity:
i. Electrical activity seen during the
insertion of the needle
ii. Normal insertional activity
typically only lasts a few hundred
milliseconds, just barely longer
than the needle movement itself
iii. Generated by depolarization of
muscle fibers due to piercing and
displacement by the needle
iv. Decreased insertional activity occurs when muscle is atrophied
v. Technique for silencing the muscle: asking the patient to
contract the antagonist muscle
vi. Increased insertional activity: precedes denervation
sometimes
Insertional Activity
b. Muscle at rest
i. Spontaneous activity:
1. Typically abnormal
2. Occurs due to damage to muscle fibers and relative
depolarization of the resting potential from -90 mV to
-60 mV (influx of Na+)
3. Types of spontaneous activity (most them with small
amplitudes)

Activity at Picture Description, Pathophysiology


Rest Sound and Etiology
Positive Primary Early
Sharp Wave deflection from Denervation
baseline
followed by Indicate
return to acute or
baseline. Mono- ongoing
or Bi-phasic.
Could be either Process of
regular or .denervation
irregular. "dull May be
thuds"
Fibrillation Single APs of Neurogenic and
muscle fibers, myopathic
regular or disease,
irregular. Usually spontaneous
triphasic. discharge due
"raindrops to impaired
hitting tin roof" innervation
Complex Group of Longstanding
Repetitive spontaneously disorders,
Discharge firing Aps. suggestive that
(CRD) Regular with the injury is
uniform greater than 6
frequency mo.
"motorboat that
misfires
occasionally"
Myotonic Either PSW or Myotonic
discharges biphasic or Dystrophy,
triphasic Myotonia
morphology. congenital,
Variable rate paramyotonia,
with waxing and hyperkalemic
waning. "Dive periodic
Bomber sound". paralysis,
polymyositis,
Prolonged firing acid maltase
after activation, deficiency,
delayed chronic
relaxation after radiculopathy
forceful and
contraction neuropathies
Myokymic Spontaneous
discharge MUAPs with
regular firing
pattern and
rhytem: (1)
continuous form
with single and
paired
discharges at 5-
10 Hz. (2)
Discontinous
form – bursts of
Aps at 0.1-10 Hz.
"soldier
marching"
Endplate When inserting
Region the needle into
Potentials: the endplate,
MEPPs both MEPPs and
endplate spike
maybe seen,
accompanying
with significant
pain. Nothing
could be
interpreted from
these potentials.
c. Analyzing the motor unit (MU): the patient is asked to minimally
contract the muscle. Components of the MU:
i. Amplitude:
1. Produced by the closest MU to the needle
2. Normal: 1 uV – 2000 uV (1 mV)
3. Increased: re-innervation (neuropathic injuries)
4. Decreased: myopathies
ii. Rise Time:
1. Time lag from the peak of the initial positive deflection
to the subsequent upward peak
2. Influenced by the distance between the recording tip
and the MU that fires.
3. Should be 0.5 msec or less, with more – reposition the
needle (technical)
iii. Duration:
1. Time from initial departure from baseline to final
return to baseline
2. Normal: 5-15 msec
3. Indicates the degree of synchrony of firing among all
individual muscle fibers with variable length,
conduction velocity and membrane excitability
4. Increased duration: neuropathic process (re-
innervation  desynchrony)
5. Decreased duration: myopathic disorders (fewer
muscle fibers contribute to the MU)
iv. Phases
1. Portion of the waveform between successive crossing
of the baseline
2. Normally, MUAP has 4 or fewer phases
3. Polyphasic MU = >4 phases. Suggests desynchronized
discharge of drop-off of individual fibers
4. If muscle have >40% (monopolar) or >20% (concentric)
polyphasic unit it is considered polyphasic
d. Recruitment:
i. Physiology:
1. The orderly addition of MUs so as to increase the force
of a contraction.
2. A contraction becomes stronger when either:
a. MUs increase their firing rate, or
b. Additional MUs commence firing
3. The patient is being asked to think about contracting
the muscle
4. Pattern of recruitment:
a. Single MU fire irregularly at 3Hz
b. Single MU fire rgulary at 5Hz
c. At 10 Hz another MU is recruited and fire at 5
Hz
5. Recruitment Ratio= maximal frequency / no. of MUs.
6. Decreased Recruitment
a. Part of the MUs are unable to fire
b. The remaining Mus try to compensate and fire
at higher frequency before other MUs are
recruited
c. Recruitment Ratio >8 suggests neurogenic
process. Firing rates > 20-30Hz
d. Etiologies: Neuropathy, Radicolopathy, MN
disease, nerve trauma
e. Frequency of firing can differentiate neurogenic
weakness from psychogenic or antalgic
weakness: for both cases few MUs will be
recruited, but for neurogenic the frequency will
be increased while for psychologic/antalgic the
frequency will remain normal
7. Increased / Early Recruitment:
a. A large number of MUs are recruited for a
minimal contraction – each MU is smaller
b. MU cannot increase their force output, so they
quickly recruit other to icrease force
c. Recruitement ratio < 3 suggest increased
recruitment
d. Etiology: Myopathy
e. MUAPs are short and of low amplitudes, firing
at increased rates
f. It is difficult to obtain one MUAP at a single
screen
8. Polyphasicity and spontaneous potentials could be
seen at both neuropathies and myopathies.
9. Only Type I MUs are evaluated because there are
recruited first and by the time Type II MUs will be
recruited the screen will be obscured by typeI MUAPs.
This is problematic for certain myopathies that
primarly affect Type II fibers, such as stroid
myopathies.

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