How can we help?

You can also find more resources in our Help Center.

EMG/NCS Study

STUDY
PLAY
Why can normal proximal sensory studies have decreased amplitude?
Phase cancelation
Why do mixed nerve studies have shorter latencies than sensory or motor studies?
Because the fastest Ia muscle spindle fibers are only recorded in mixed nerve studies.
What is the slowest speed that a normally myelinated nerve can have?
35 m/s
What is the longest latency when compared to the upper limit of normal that a normally myelinated nerve can have? Hint %.
130%
How do axonal lesion affect the waveform?
They decrease the amplitude and can mildly slow the conduction velocity, but never below 35 m/s.
What types of lesion decrease waveform amplitude?
Axonal and demyelinating lesions with conduction block. Amplitude can also decrease due to increased phase cancellation with demyelination in sensory nerves.
What is the name for the pattern seen in NCS performed within 3 days of a nerve transection (i.e. hyperacute)?
Pseudo-conduction block, because the waveform is normal distally and has decreased amplitude when stimulated proximally.
When does Wallerian degeneration begin after a nerve injury in motor fibers and sensory fibers?
Earlier in motor fibers at 3-5 days and in sensory fibers 6-10 days.
What are the conduction velocity cutoff values for the arms and legs that signify almost undoubtly that a lesion is demyelinating?
35m/s in the arms and 30m/s in the legs
What is the % drop in CMAP that signifies conduction block?
20% decrease with proximal stimulation in either area or amplitude. But many use 50% as the cutoff because this is the upper limit to where temporal dispersion alone can drop the CMAP amplitude.
How do you use conduction block to differentiate between inherited and acquired neuroapathies?
Inherited neuropathies have uniform demyelination i.e. CMT and have slowing, but not conduction block where acquired such as GBS or CIDP have focal patchy demyelination causing conduction block.
What is normal F-wave persistence?
>50%
I what scenario may absent F-waves be normal?
In a sleeping or sedated patient.
Why do you turn the stimulator with anode away from the recording electrode for F-waves?
There is a theoretical possibility of anodal block, where the nerve is thought to hyperpolarize anode blocking antidromic transmission of the shock.
What cells create the F-wave?
Differing small populations of anterior horn cells (which is why F-waves vary from stimulation to stimulation).
What are 2 troubleshooting tests when F-waves are absent?
Assure supramaximal stimulation and the Jendrassk maneuver of clench teeth or making a fist with the contralateral hand to "prime" the anterior horn cells.
When tibial F-waves are absent, have decreased persistence, increased chronodispersion, or have prolonged latencies, what may this indicate?
A S1 radiculopathy or polyneuropathy, due to any cause even an acute neuropathy i.e. early AIDP.
Why is height of the patient an important consideration when interpreting F-wave latencies?
The latency is determined by factoring in the length of the nerve, so if a person is abnormally tall a prolonged F-wave latency may be normal.
How do you estimate the length from the stimulation site to the spinal cord when determining the F-estimate?
For tibial/peroneal studies you measure from the xiphoid to the ankle stimulation site and for the median/ulnar studies you measure from the C7 spinous process to the stimulation site.
What is the F-estimate equation?
F (latency) estimate= 2(D/CV)*10+1ms+DL, where D is the distance to hte spinal cord, CV is conduction velocity in m/s, 10 is the time conversion factor to ms, 1ms is "turnaround time" in the spinal cord, and DL is the distal motor latency in ms.
What can be diagnosed by abnormal F-waves?
A proximal neuropathy (AIDP), plexopathy, or radiculopathy.
What spinal levels are tested with the different F-waves?`
Median/ulnar: C8 and T1 (so if you have a C8 radiculopathy F-waves will be normal due to the T1 component).
Peroneal: L5
Tibial: S1
How are H-reflexes different from F-waves in their most basic sense?
H-reflexes involve a synapse and are therefore true reflexes whereas F-waves do not and H-reflexes are sensory responses where F-waves are motor responses.
Describe what creates an H-reflex?
Long duration, submaximal stimulation selectively activates the Ia muscles spindle nerve fibers of the afferent S1 reflex arc
What happens to the H-reflex as stimulation intensity increases?
The H-reflex's amplitude decreases as the M-wave increases as more muscle fibers become stimulated covering or blocking the descending H-reflex.
What is an axon reflex?
It is a late potential that is sometimes present between the M wave and F waves when recording F waves that look the same when ever they occur in time and shape.
What is the cause of the axon reflex?
It is caused by reinnervation and the firing of these reinnervated sprouts.
Why is it important to recognize A reflex waves?
Because they typically only occur at submaximal stimulation (so if you're recording F-waves you should be supramaximal), they are an indicator of reinnervation, and for unknown reasons they are often seen during the 1st several days in GBS.
What is tested with the blink reflex?
CN V, CN VII, and their connections in the pons and medulla
What clinical exam finding is the correlate to the blink reflex?
The corneal blink reflex
What is the afferent and efferent limb of the blink reflex?
Afferent= V1 and CN V nucleus
Efferent= Nucleus and tract of VII
What do R1 and R2 represent in the blink reflex?
R1=Disynaptic reflex between the CN V nucleus ipsilateral to stimulation and the ipsilateral CN VII nucleus. R1 is always present.

R2=Multisynaptic pathway btw CN V and ipsilateral/contralateral CN VII nucleus. These are variable and extinguish with repeated stimulation.
What is measure with blink reflex?
First whether or not there is a signal, the latencies of ipsilateral R1 and bilateral R2's, and the latencies differences btw R1's and the difference btw R2's.
What is the use of the blink reflex?
It can help localize lesions to the trigeminal nerve, facial nerve, pons, medulla, or a general demyelinating lesion based on R1 and R2 latencies and patterns.
What is the physiology of 2-3Hz slow repetitive stimulation?
ACH is incrementally depleted from the primary store, so fewer quanta (ACH vesicles) are released into the cleft with each stimulation, however there are still sufficient amounts of ACH to bind with ACHR to stay above the end plate potentials "safety factor" and cause the all of nothing depolarization of all muscle fibers controlled at that NMJ.
What is the physiology of 10-50Hz rapid repetitive stimulation?
In this the ACH is depleted and the primary quanta are repleted with the secondary stores like with slow rep. stim, but also Ca in the presynaptic cleft builds up because the rapidity of the stim. cause Ca influx faster than it can be pumped out, thus increase the ACH that is ultimately released increasing the end plate potential way above the safety threshold at first, so the subsequent drop of ACH due to using up the quanta does not affect the muscle depolarization.
How does decrement with slow rep stim and increment in rapid rep stim when done after slow rep stim. occur in NMJ diseases?
In NMJ diseases there is less safety factor and not much reserve, so with slow rep. stim. as less ACH is released you get the decrement and then with rapid rep. stim. you greatly increase the amount of ACH that is released increasing the safety factor causing more muscle depolarization and the increment.
4 key things to describe in EMG report
- location
- duration
- severity
- prognosis
What is the basic functional element of the neuromuscular system?
the motor unit
What are the 7 components of the motor unit (from proximal to distal)?
- anterior horn cell
- nerve root
- spinal nerve
- plexus
- peripheral nerve
- neuromuscular junction
- muscle fiber
Where is the alpha-motor neuron located?
cell body of the motor nerve; located in the anterior horn of the spinal cord
What regulates the characteristics of the motor unit?
The alpha motor neuron
What is the innervation ratio?
The amount of muscle fibers belonging to an axon
Do muscles with stronger/grosser movements have a higher or lower innervation ration?
Higher (more muscle fibers per axon)
What is the relationship between innervation ratio and force generated by a muscle?
Higher innervation ratio = greater force
What is a typical innervation ratio for a muscle in the leg?
600 muscle fibers : 1 neuron
What is a typical innervation ratio for a muscle around the eye?
1 muscle fiber : 1 neuron
Define the neuromuscular junction
The location in the motor unit where electrical AP is converted to chemical energy to initiate a a muscle action potential.
What type/category of motor neurons can can EMG study?
Alpha motor neurons (Ia fibers)
What are the 2 general ways that alpha motor neurons are further described?
- size
- physiology
What order are alpha motor neurons recruited?
In order of the size of the motor unit (smaller muscle fibers first)
The sequential activation of motor units allowing for smooth increase in contractile force is described by what principle?
Henneman Size Principle
Alpha motor neurons innervate ______
extrafusal fibers (skeletal muscle)
Gamma motor neurons innervate ______
intrafusal fibers (muscle spindle)
Beta motor neurons innervate _____
intrafusal and extrafusal fibers (skeletal muscle and the muscle spindle)
What are extrafusal fibers?
skeletal muscle
What are intrafusal fibers?
muscle spindle fibers
4 basic characteristics of type I muscle fibers
- smaller cell body
- thinner diameter axon
- lower innervation ratio
- slower twitch muscle
4 basic characteristics of type II muscle fibers
- larger cell body
- thicker diameter axon
- higher innervation ratio
- faster twitch muscle
What is the Henneman size principle?
A smaller alpha motor neuron has a lower threshold of excitation causing it to be recruited first. Larger alpha motor neurons have larger thresholds causing them to be recruited when more force is needed.
What order do the "neurium" layers go in from outside in?
- epineurium
- perineurium
- endoneurium
Define endoneurium
Connective tissue surrounding each individual axon and its myelin sheath
Define perineurium
Connective tissue surrounding bundles or fascicles of myelinated and unmyelinated nerve fibers
What is the purpose of the perineurium?
- strengthens the nerve
- acts as a diffusion barrier
May individual neurons cross from one bundle to another throughout the course of the nerve?
yes
Define epineurium
loose connective tissue surrounding the entire nerve that holds the fascicles together and protects it from compression
Define resting membrane potential
the voltage of the axon's cell membrance at rest
What are "leak channels"?
Channels that allow K and Na to move passively in and out of the cell membrane
What is the normal resting membrance potential of an axon?
-70 to -90mV
How many K and Na are involved in the K/Na pump?
3Na out for every K in
The resting membrane potential is maintained by the
Na/K pump
Most important event in generating an action potential is...
sodium conductance
How does the stimulator in NCS cause the nerve to depolarize?
Positive ions accumulate under the negative pole of the stimulator (cathode) and lower the membrane potential. The membrane becomes increasingly permeable to Na ions which eventually rush in through the voltage gated channel and depolarize the membrane (sodium conductance)
What are the 3 conformations of the voltage gated sodium channel?
- resting
- activated
- inactivated
About how long to sodium channels stay open during an action potential?
about 25 microseconds
What are the general conceptual effects of cold on the sodium channel?
channel open and closes later
Is there a difference in the waveform effects in NCS for focal vs. generalized cooling?
Yes, generalized cooling has more significant effects in all domains
Classically, cooling causes an increase in the amplitude of NCS - but sometimes you see a decrease...why?
- temporal dispersion
- negative phase cancellation
What are the general effects of cooling that can be expected with NCS waveform morphology?
- latency prolonged
- amplitude increased
- duration increased
- conduction velocity decreased
Why does the movement of Na into a channel end up causing a propagating action potential?
Because the path of least resistance is along the length of the axon (both directions)
During an action potential when sodium is rushing in - what prevents it from going right back out
myelin
The process of propagating a current from one node to another is called
saltatory conduction
Define orthodromic
action potential is monitored traveling in the direction of its typical physiology conduction (usually described as away or toward the spinal cord)
Define antidromic
action potential is monitored traveling in the opposite direction of its typical physiology conduction (usually described as away or toward the spinal cord)
The repolarization phase of an action potential is dependent on
Na channel inactivation and K channel activation
What are the 2 conformational phases of the voltage gated K channels?
- resting
- slow activation
What is the "overshoot phenomenon"?
The hyperpolarization that occurs because of the slow activation of K channels
What is the motor endplate?
The distal portions of the motor axon and the muscle fibers that they innervate
Define the presynaptic region of the neuromuscular junction
the bulbous area at the axon's terminal zone
How many storage compartments are there for acetylcholine in the presynaptic region of the axon and how many quanta does each compartment store?
- main store = 300,000
How long does the migration of acetylcholine from the axon's main and mobilization compartments to immediate release take?
4-5 seconds
Define the synaptic cleft of the region of the neuromuscular junction in a motor neuron
the regions where acetylcholine crosses from the presynaptic region towards receptors on the postsynaptic region
How wide is the synaptic cleft of the neuromuscular junction?
about 200-500 angstroms
Acetylcholinesterase degrade acetylcholine into...
Acetate and choline
The convolutions in the postsynaptic region increase the surface area by how many times
10
What are "presynaptic active zones" in the motor neuron?
Areas on the presynaptic membrane where acetylcholine is released
The postsynaptic Ach receptor requires __ molecules of Ach to be activated
2
During the periods of inactivation in a motor unit, a spontaneous release of Ach quanta occurs every __ seconds
5
Spontaneous release of Ach quanta in motor neurons results in ____
MEPP (miniature endplate potential)
The calcium associated with depolarization and release of Ach in motor neurons stays in the terminal axon for how long?
200ms
Normally, the end-plate potential amplitude is ___ times amount needed to initiate an action potential
4
The "safety factor" in an end-plate potential depends on what 2 factors
- quantal count (numbner of quata released)
- quantal response (ability of receptors to respond)
What are the defining edges of the sarcomere?
Z line to Z line
During normal muscle contraction the I band and the H zone ____ in size
decrease
During maximal muscle contraction the H zone...
disappears
Muscle contraction is initiated by
muscle fiber depolarization
How quickly does muscle fiber depolarization spread?
3-5 meters per second
How can the muscle fiber depolarization penetrate deeper into the muscle?
T-tubule system (calcium is released from the sarcoplasmic reticulum)
What is Ohm's law?
E = IR

Electromotor source (volts)
Current (I) amperes
Resistance (Ohms)
CMAP =
compound muscle action potential
SNAP =
sensory nerve action potential
What are the limitations of using a needle recording electrode in NCS?
Because you are only recording a few fibers you can't validly analyze the amplitude or the conduction velocity of the waveform you record with a needle.
Describe a monopolar electrode. Where is the reference?
22-30 gauge Teflon coated needle with exposed tip of 0.15-0.2mm
- requires external reference
What are the advantages of the monopolar electrode?
- inexpensive
- conical tip allows for omnidirectional recording
- less painful
- larger recording area
- records more positive sharp waves
What is the relative recording area size of monopolar vs. concentric needles?
monopolars record twice as much field
What are the disadvantages of monoplar electrodes?
- requires a separate reference
- unstandardized tip area
- Teflon can fray
- more interference
Describe a concentric electrode. Where is the reference?
The 24-26 gauze needle serves as the reference, the active is a bare inner wire
What are the advantages of the concentric electrode?
- standardized active area
- fixed location from the reference
- less interference
- no separate reference
- can be used for quantitative EMG
What are the disadvantages of the concentric electrode?
- beveled tip = unidirectional recording
- smaller recording are
- MUAPs have smaller amplitudes
- more painful
MUAP =
motor unit action potentials (what you see on EMG)
Describe a bipolar concentric electrode
Has active and reference electrode wires within the needle lumen
Define ground electrode
A zero-voltage, neutral, surface reference point placed between the recording electrode and the stimulating electrode
Define anodal block
A theoretical local block that occurs when reversing the stimulator's cathode and anode; this hyperpolarizes the nerve, thus inhibiting the production of the action potential.
Define threshold stimulus
electrical stimulus occuring at an intensity level just sufficient enough to produce a detectable evoked potential from the nerve
Define maximal stimulus
Electrical stimulus at an intensity level where no further increase in evoked potential occurs as a higher stimulus
Define supramaximal stimulus
20% above maximal stimulus
What effect does supramaximal stimulus have on latency?
Decreased
What technical NCS error can occur with stimulus duration greater than 0.3ms?
falsely prolonged distal latency since nerve is stimulated for a longer period of time
Recommended stimulus duration in NCS
0.1-0.3ms
6 sources of environmental electrical noise interference in EMG/NCS
- EMG audio feedback
- needle artifact
- 60Hz interference
- preamplifier
- fluorescent lights
- the patient
Signal to noise ratio =
(signal amplitude) x (square root # averages performed) / noise amplitude
Stimulus artifact represents
the current spread across the skin to the electrode
List 3 ways you can reduce the stimulus artifact
- ground between the stimulator and recording electrode
- appropriate anode and cathode placement
- improving electrode contact by cleaning the skin
What does the differential amplifier do?
- responds to alternating currents
- cancels waveforms recorded at active and reference pickups
- amplifies remaining potentials
Optimal parameters for a differential amplifier
- high impedance
- common mode rejection
- low noise from within the system
What's an acceptable common mode rejection ratio (CMRR)?
Greater than 90dB
What does the common mode rejection ratio tell you?
The larger the CMRR the more efficient the amplifier
NCS: Differential signal =
active - reference
Filters are made of
resistor and capacitors
What is the frequency band width in electrodiagnostics?
The frequencies between the low and high frequency filters that the machine is allowed to see
What are the typical filter settings for sensory NCS
20Hz - 2kHz
What are the typical filter settings for motor NCS
2Hz-10kHz
What are the typical filter settings for EMG?
20Hz-10kHz
What effects on waveform morphology occur with elevating the low frequency filter
- shortens peak latency
- reduces the amplitude
- potentials go from bi- to triphasic
- does not change the onset latency
What effects on waveform morphology occur with reducing the high frequency filter
- prolongs the peak latency
- reduces amplitudes
- creates a longer negative spike
- prolongs the onset latency
What are the x and y axes on the screen display for NCS
x = sweep speed
y = sensitivity
NCS sweep speed is measured in
ms
NCS sensitivity is measured in
mV or uV
In NCS what are the units of gain?
no units; it's a measurement of output to input
Why does demyelination cause problems with saltatory conduction?
Demyelination increases the membrane capacitance (loss of insulation)
Define conduction block
Failure of the action potential to propagate past an area of demyelination along the structurally intact axons
What are the parameters for defining conduction block on NCS?
greater than 50% amplitude drop
Typical NCS findings with demyelination
- prolonged latency
- decreased amplitude across the site of injury
- temporal dispersion
- decreased conduction velocity
Typical EMG findings with demyelination
- normal insertional activity
- normal resting activity +/- myokymia
- +/- decreased recruitment
- MUAP normal
What changes with demyelination?
- shorter internodal distance
- conduction velocity improves but still slower than normal
When is Wallerian degeneration complete for motor nerve and sensory nerves?
- motor complete by 7 days
- sensory complete by 11 days
4 general mechanisms of axon injury
- focal crush
- stretch
- transection
- peripheral neuropathy
Typical NCS findings with axonal injury
- normal latency
- decreased amplitude in the entire nerve
- normal temporal dispersion
- decreased conduction velocity
Typical EMG findings with axonal injury
- abnormal insertional activity
- abnormal resting activity
- decreased recruitment
- abnormal MUAP
2 major mechanisms of recovering after axonal injury
- collateral sprouting
- axonal regrowth
How fast will an axon regrow?
1mm/day; 1 inch/month
What are nascent potentials?
motor units after axonal regrowth that have low amplitude, long duration and are polyphasic
What is the Seddon classification?
Seddon classification of nerve injury:
- neuropraxia (compression)
- axonotmesis (crush)
- neurotmesis (transection)
What is the Sunderland classification?
Sunderland classification of nerve injury:
Type 1: conduction block (neuropraxia)
Type 2: axonal injury (axonotmesis)
Type 3: type 2 + endoneurium injury
Type 4: type 3 + perineurium injury
Type 5: type 4 + epineurium injury (neurotmesis)
A recorded potential on NCS is made up of
multiple sinusoidal waves
Frequency in NCS is measured in
Hz
Define onset latency
The time required for an electrical stimulus to initiate an evoked potential
Define latency of activation
The time between initiation of the electical stimulus and the beginning of saltatory conduction
Typical duration of latency of activation
0.1ms or less
Typical time for synaptic transmission
0.2-1.0ms
Onset latency in NCS represents
Conduction along the fastest axons
Define how you measure onset latency
Initial deflection from baseline
Peak latncy in NCS represents
conduction along the majority of axons
General parameters for normal conduction velocities in the upper and lower limbs
- upper 50 m/s
- lower 40 m/s
How can conduction velocities be normal even with a lot of axon loss?
Intact transmission in the fastest fibers
General guidelines for conduction velocities in children
- newborns: 50% of adults
- 1 year old: 80% of adults
- 3-5 years: equal to adults
General guidelines for how nerve conduction decreased witha ge
Decreased 1.5% per year after age 60 years
What does amptliude reflect in NCS (generally)
The number of nerve fibers activated and their synchrony of firing
What does temporal dispersion in NCS tell you?
The range in conduction velocities of the fastest and slowest axons (usually seen better with proximal stimulation)
An amplitude drop of up to ___ is considered normal for proximal SNAPs
50%
Why is there so much amplitude drop with proximal SNAP stimultion?
Phase cancellation; more pronounced with short duration SNAPs
Expected ampltiude drop in proximal stimulation for CMAPs
About 15%
Location of the dorsal root ganglion
In the neural foramen
Which is more sensitive in detecting an incomplete peripheral nerve injury, SNAPs or CMAPs?
SNAPs
Features of antidromic sensory studies
- easier to records than orthodromic
- require less stimulation than ortho
- have larger ampltiudes than ortho (nerves are more superficial distally)
For SNAPs the active and recording electrodes should be at least ___ cm apart
4
How does waveform morphology change when the active and reference electrodes are less than 4cm apart?
- peak latency decreases
- onset latency about the same
- amplitude decreases
- duration decreases
- rise time deceases
Why can't motor NCS localize pre- vs post-ganglionic lesions?
Because the cell body is in the spinal cord
List 2 reasons to have a nerve with normal SNAPs but abnormal CMAPs on NCS
- motor lesion proximal to the DRG
- lesion of only the motor fibers
What is the general normal waveform appearance for CMAPs?
- biphasic
- initial negative deflection
3 major reasons to see an initial positive deflection on CMAP waveform
- active electrode not over motor point
- volume conduction from other muscles/nerves
- anomalous innervation
What amplitude measure do you use for SNAPs
peak to peak
What amplitude measure do you use for CMAPs
baseline to peak
The H-reflex is an electrically evoked analogue to a ______
monosynaptic reflex
What kind of stimulus do you use for H-reflex?
submaximal with long duration (0.5ms-1.0ms)
What do you us a submaximal long duration stimulus for H-reflex studies?
This preferentially activates the IA afferent fibers
What kind of responses are involved in the H-reflex?
orthodromic sensory response to the spinal cord and an orthodromic motor response back to the recording electrode
How can you facilitate the H-reflex?
agonist muscle contraction
How can you abolish the H-reflex?
- Antagonist muscle contraction
- Supramaximal stimulation that causes "blocking"
Are the morphology and latency of H-reflex waveforms constant or variable?
constant at the appropriate stimulus
What is the "formula" for H-reflex?
= 9.14 +0.46 (leg length in cm from the medial malleolus to the popliteal fossa) +0.1 (age)
What is the generally normal latency for H-reflex? side to side difference? changes with age?
- latency: 28-30ms
- side to side difference: greater than 1-2 ms
- above 60 years: add 1.8ms
Trace the fibers traveled for the H-reflex
1A afferent --> synapse in spinal cord to --> alpha motor neuron
What are the 2 muscles typically studied with H-reflexes?
- gastrosoleus (tibial motor, S1)
- flexor carpi radialis (median motor, C6-7 pathway)
In what groups of patients can H-reflexes be obtained in almost any muscle group?
- infants
- adults with UMN corticopinal tract lesions
List some common limitations of the H-reflex
- evaluates a long pathway which can dilute focal effects
- can be normal with incomplete lesions
- does not distinguish between acute and chronic lesions
- once abnormal, always abnormal
What stimulation level do you use for F-waves?
supramaximal
What is the general pathway for an f-wave?
antidromic motor to the spinal cord with orthrodromic motor return
What is the approximately amplitude of an f-wave compared to the CMAP?
5%
Is the f-wave latency constant or variable? why?
variable. It's a polysynaptic response where renshaw cells can have an inhibitory effect
Normal UE latency for f-waves
28msec
Normal LE latency for f-waves
56msec
What is the significant side-to-side difference for f-waves?
2.0msec in UE, 4.0msec in LE
Limitations of the f-wave
- evaluates a long pathway which can dilute focal lesions
- only assess motor fibers
What happens to a-waves with supramaximal stimulation?
They disappear
General location of an a-wave on a trace
Between with CMAP and the f-wave at a constant latency
what does an a-wave represent?
Usually collateral sprouting
On NCS the blink reflex is likely what reflex on physical exam?
the corneal reflex
What nerves are tested in the blink reflex in NCS?
V and VII
Trace the pathway being tested during the blink reflex
sensory of superorbital branch of trigeminal nerve (VI) --> pons --> lateral medulla --> facial nerve (VII) --> bilateral orbicularis oculi
The R1 response in the blink reflex NCS represents a pathway through the
pons
The R2 response in the blink reflex NCS represents a pathway through the
pons and lateral medulla
The R1 response in the blink reflex NCS is affected by lesions of the...
- trigeminal nerve
- pons
- facial nerve
The R2 response in the blink reflex NCS is affected by lesions of the...
- consciousness level
- Parkinson's disease
- lateral medullary syndrome
- contralateral hemisphere
- valium
- habituation
What are the normal latency measurements for the blink reflex?
R1 < 13 msec
R2 ispilateral <40 msec
R2 contralateral <41msec
Where do you stimulate and record for a facial nerve NCS?
- stim distal to the stylomastoid foramen at the angle of the mandible
- record over nasalis
Common manifestations of synkinesis after facial nerve injury
- lip twitching when closing the eye
- eye closure when smiling
- crocodile tears when chewing
Give some of the more common underlying causes of a facial nerve lesion
- bell's palsy
- neoplasms
- fractures
- middle ear infections
- DM
- Lyme disease
If you want to follow-up facial NCS to look at prognosis, how far apart should the studies be?
OK to f/u every 2 weeks or so
How can you use evoked potentials of the facial nerve to predict prognosis?
Absence of evoke potentials at 7 days indicate poor prognosis
Describe facial nerve recovery prognosis based on CMAP amplitude
- less than 10% of unaffected side = poor (recovery often greater than 1 year and likely incomplete)
- 10-30% of unaffected side = fair (recovery within 2-8 months)
- >30% unaffected side = good (recovery within 2 months)
Common interventions to try for facial nerve palsy
- prednisone
- massage
- estim
What path in the spinal cord does SSEP test?
posterior columns
Trace the ascending pathway for SSEPs
peripheral nerve --> plexus --> root --> spinal cord (posterior column)--> contralateral medial lemniscus --> thalamus --> somatosensory cortex
What level of stimulus is used for SSEPs?
repetitive submaximal stim
In general, how are SSEPs utilized for surgical monitoring during lumbar spine surgery
if tibial signals are lost and median signals stay intact it is concerning for injury during spine surgery
List the N_ labels / recording sites commonly used for SSEP with median nerve stimulation
- N9: Erb's point
- N11: Roots
- N13: Cervical medullary junction
- N20: Cortical
List the N_ labels / recording sites commonly used for SSEP with tibial nerve stimulation
- PF - popliteal fossa
- L3 - 3rd lumbar
- N22: T12 / lumbosacral spine
- N45: cortical
What sensation travels in the dorsal columns?
- vibration
- proprioception
List major limitations of SSEPs
- only tests dorsal columns
- evals a long pathway and may dilute focal lesions
- adversely affected by sleep, high dose general anesthetics
Normal insertional activity on needle EMG is
300ms
2 main causes of increased insertional activity on needle EMG
- denervation
- irritable cell membrane
4 main causes of decreased insertional activity on needle EMG
- fat
- fibrosis
- edema
- electrolyte abnormalities
End plate potentials on needle EMG represent
single fiber action potentials
Spontaneous quanta release at the NMJ occur about every __ seconds
5
What causes a miniature endplate potential (MEPP) on needle EMG?
spontaneous release of Ach quanta
Describe the appearance of MEPPs on needle EMG
10-50uV non-propagated potential - generally appears as an irregular baseline
MEPPs are usually ____-phasic
mono
EPPs are usually ___-phasic
biphasic
Typical duration of a MEPP
0.5-1.0ms
Typical duration of an EPP
2.0-4.0ms
Typical amplitude of a MEPP
10-50uV
Typical amplitude of an EPP
less than 1mV
Typical rate of firing of MEPP
150Hz
Typical rate of firing of EPP
50-100Hz
Firing rhythm of a MEPP
irregular
Firing rhythm of an EPP
irregular
Origin of the MEPP
endplate
Origin of the EPP
enplate/provoked with mechanical depolarization
Typical sound of a MEPP
Sea shell murmur
Typical sound of an EPP
sputtering fat in a frying pan
What is the underlying pathophysiology of a fibrillation?
denervated single muscle fibers from uncontrolled ACh release
Firing rhythm of fibrillations
regular
Why don't positive sharp waves have a negative phase?
because they are propagated to but not beyond the needle tip
The initial deflection of a fib is
positive
The initial deflection of a PSW is
positive
Typical duration of a fib is
1-5ms
Typical duration of a PSW
10-30ms
Typical amplitude of fib
early is greater than 300uV and late is less than 25uV
Typical amplitude of PSW
less than 1mV
Typical rate of firing of a fib
1-10Hz
Typical rate of firing of a PSW
1-20 Hz
Firing rhythm of a fib
regular
Firing rhythm of a PSW
regular
Is the origin of the fib pre- or post-unctional?
postjunctional
Is the origin of the PSW pre- or post-unctional?
postjunctional
Typical sound description of a fib
rain on a tin roof
Typical sound description of a PSW
dull thud or chug
Define 0 fibs/PSW
none
Define 1+ fibs/PSW
Persistent single runs >1 second in 2 areas
Define 2+ fibs/PSW
Moderate runs greater than 1 second in three or more areas
Define 3+ fibs/PSW
Many discharges in most muscle regions
Define 4+ fibs/PSW
Continuous discharges in all areas of the muscle
How are complex regional discharges (CRDs) generated?
AP generated from a single pacemaker that causes a group of single muscle fibers to fire in synchrony
Typical amplitude of a CRD
50-10000uV
Typical rate of firing of a CRD
10-100Hz
Typical rhythm of firing of a CRD
Regular spurts with abrupt starts and stops
Origin of a CRD
postjunctionall/ephaptic transmission
Typical sound description of a CRD
motor boat
Classic causes of CRDs
- anterior horn cell diseases
- chronic radiculopathy
- peripheral neuropathy
- polymyositis
- dermatomyositis
- musclar dystrophy
- limb girdle dystrophy
- myxedema
* can be normal variant
Typical duration of a myotonic discharge
5-20 ms
Typical amplitude of a myotonic discharge
20-300uV
Typical rate of firing of a myotonic discharge
20-100Hz
Typical rhythm of a myotonic discharges
wax and wane
Origin of a myotonic discharge
postjunctional
Typical sound of a myotonic discharge
dive bomber
Classic diseases where myotonic discharges are found
- chronic radiculopathy
- peripheral neuropathy
- myotonic dystrophy
- myotonia congenita
- paramyotonia
- polymyositis
- dermatomyositis
- maltase deficiency
- hyperkalemic periodic parlysis
- propranolol
Hallmark sign of a fasciculation
irregularly firing motor unit
Typical duration of a fasciculation
5-15ms
Typical amplitude of a fasciculation
less than 300uV
Typical rate of a fasciculation
0.1-10Hz
Typical rhythm of a fasciculation
irregular
Origin of a fasciculation
prejunctional
Describe grade 0 fasciculation
none
Describe grade 1+ fasciculation
In 2 areas, 2-10/min
Describe grade 2+ fasciculation
In many areas, 10-15/min
Describe grade 3+ fasciculation
All areas, < 60/min
Describe grade 4+ fasciculation
All areas >60/min
What are myokymic discharges?
groups of MUAPs firing repeatedly
Typical amplitude of myokymic discharges
100uV to 2mV
Typical rate of myokymic discharges
discharge 40-60Hz, interdischarge 0.1-10Hz
Typical rhythm of myokymic discharges
semiregular
Origin of myokymic discharges
prejunctional
Typical sound of myokymic discharges
marching soldiers
Typical causes of facial myokymia
MS, brainstem neoplasms, polyradiculpathy, Bell's palsy
Typical causes of myokymia in the extremities
radiation plexopathy, compression neuropathy, rattlesnake venom
When are neuromyotonic discharges classically seen?
neuromyotonia (Isaac's syndrome)
Why do neuromyotonic discharges taper off at the end?
because the single muscle fiber firing fatigues
Duration of neuromyotonic discharges
variable can be continuous or in bursts
Characteristic amplitude of neuromyotonic discharges
progressive decrement
Typical rate of neuromyotonic discharges
100-300Hz
Typical sound of neuromyotonic discharges
Ping or motorcycle
Waveform appearance of a neuromyotonic discharges
tornado
Typical duration of a cramp discharge
gradual start and stop
Typical amplitude of a cramp discharge
up to 1mV
Typical rate of cramp discharge
40-150Hz
Typical rhythm of cramp discharge
irregular
Causes of cramp discharge on EMG
- salt depletion
- uremia
- pregnancy
- myxedema
- prolonged muscle contraction
- myotonia congenita
- myotonic dystrophy
- stiff-man's syndrome
What's the difference between "noise" in an EMG study and artifact potentials?
noise is external to the system, artifact potentials are internal to the system
What's a MUAP?
An action potential from muscle fibers belonging to a single motor unit within the recording range of the electrode (5-15mm)
Normal amplitude of a MUAP
1mV
What does the rise time represent?
The proximity of the needle to a motor unit
What's normal rise time for motor unit on needle EMG?
less than 500us
Normal MUAP duration
5-15ms
Turns on MUAP are also called
serrations
How do you calculate the phasicity of a MUAP?
baseline crossing plus 1
How do you define polyphasicity in a motor unit?
more than 5 crossing the baseline
What % of normal adults have polyphasic motor units?
- concentric = 15%
...
- monopolar = 30%
When are doublet/multiplet potentials seen?
- ischemia
- hyperventilation
- tetany
- motor neuron diseases
- metabolic diseases
What amplitude is considered a "giant" potential?
greater than 5mV
What is the "rule of 5s" for motor units?
Tend to recruit a new motor unit in every 5Hz of firing
Describe "early recruitment" on EMG
many motor units start firing early with activation (hard to fire just one unit)
Describe "decreased" recruitment on EMG
One unit firing fast, unable to bring in additional units
What is the recruitment frequency?
The firing rate of the first motor unit when the second unit starts to fire
What's a normal recruitment frequency?
Less than 20
Recruitment frequency greater than 20 typical reflects...
Neuropathic process
What is a recruitment interval on EMG?
the interspike interval (in ms) between two discharges of the same MUAP when a second MUAP begins to fire
What's a normal recruitment interval?
100ms
How do you calculate recruitment ratio on EMG?
Firing rate of 1st MUAP / # MUAP
What's a normal recruitment ratio?
Les sthan 10
What's an interference pattern on EMG?
the electrical activity recorded from a muscle during maximum voluntary contraction
A quata of acetylcholine contains about how many molecules of acetylcholine?
5,000-10,000 molecules
Define orthodromic
when impulse travels the same way it would physiologically
Define antidromic
when impulse travels opposite the way it would physiologically
4 major uses for electrodiagnostics (reasons to order)
1. diagnosis
2. localization
3. help determine treatment
4. prognosis
3 major types of EMG needles
1. monopolar
2. bipolar
3. concentric
Role of filters (most generally)
faithfully reproduce the signal you want while trying to exclude both high and low frequency electrical noise
As sensitivity is increased, onset latency
decreases
Typical conduction velocity in a myelinated nerve
40-70 m/sec
Typical conduction velocity in an unmyelinated nerve
1-5 m/sec
Conduction block = neur____
neurapraxia
Conduction slowing and conduction block are indicative of
demyelination
Normal conduction velocity in upper extremity (general)
50 m/sec
Normal conduction velocity in lower extremity (general)
40 m/sec
CMAP amplitude is dependent on these 3 general factors
1. integrity of the axons
2. muscle fibers depolarized by axons
3. conduction velocity of individual fibers
Motor nerve amplitudes are measured in
microvolts
Sensory nerve amplitudes are measured in
millivolts
Is temporal dispersion seen in congenital neuropathies?
not usually
True or false, in general the cathode is placed towards the direction of stimulation?
TRUE
Optimal separation distance for active and reference electrodes in SNAPs
3-4cm
General placement of the ground electrode
between the stimulation and the recording electrode
In H-reflex we use _____maximal stimulation
sub
What happens to the H-reflex with supramaximal stimulation
it dissapears (replaced by M-wave)
H-reflexes in S1 are often absent in normal individuals over the age of ___
60
Formula for the f-wave ratio
(F-wave latency - CMAP latency) - 1ms/(CMAP latency x2)
Normal F-wave ratio in upper limb
1.0 +/- 0.3
Normal F-wave ratio in lower limb
1.1 +/- 0.3
An f-wave ratio higher than 1.3 indicates
a proximal lesion
An f-wave ratio lower than 0.7 indicates
a distal lesion
For motor studies, normal stimulation site differences for amplitude may be around ___
20%
How can you verify that a low amplitude is from segmental demylination and resultant temporal dispersion?
the area under the curve should be unchanged
Skin measurements appear to be accurate to about what factor?
1cm
How can you estimate the % of axonal motor loss?
Compare the amplitude to the other side
When stimulating the ulnar nerve, the elbow should be
flexed 70-90 degrees
Type of synapse in the H-reflex
monosynaptic (or oligosynaptic)
Type of synapse in the F-wave
polysynaptic
Sensory and motor pathway directions in H-reflex
Sensory orthodromic
Motor antidromic
Sensory and motor pathway directions in F-wave
Motor antidromic
Motor othodromic
Stimulus required in H-reflex
submaximal
Stimulus required in F-wave
supramaximal
Where can the H-reflex be normally elicited?
soleus
flexor carpi radialis
Where can the F-wave be normally elicited?
most muscles (distal preferred)
Where is the stimulus cathode places for the H-reflex?
proximal
Where is the stimulus cathode places for the f-wave?
proximal
What is the size of the H-reflex compared to the m-wave?
large
What is the size of the F-wave compared to the m-wave?
small
What facilitates the H-reflex?
* anything that increases motor-neuron pool excitability (contraction, CNS lesion)
What facilitates the f-wave?
facilitation does not apply here
Two major uses of the H-reflex
S1 radiculopathy
Guillain-Barre'
3 major uses of the F-wave
Demyelinating polyneuropathies
Guillain-Barre'
Proximal nerve/root injury
Reproducibility of the H-reflex
latency and configuration reproducible, amplitude varies depending on stimulation
Reproducibility of the F-wave
variable in amplitude, latency and configuration
What's the general guide for upper limit of ok side-to-side difference for H-reflex?
>1.5msec
What's the general guide for upper limit of ok side-to-side difference for f-wave in hand, calf and foot?
hand: >2 msec
calf: >3 msec
foot: > 4 msec
What do F-wave ratios assume for distance?
That the distance of stimulation is halfway between distal site and spinal cord (elbow or knee)
Overall muscle contraction is from _____fusal fibers
extrafusal
Intracellular resting potential of extrafusal fibers
-80mV
Fundamental structure assessed during EMG
the motor unit
What makes up a motor unit?
Anterior horn cell; axon; all muscle fibers that that axon innervates
Motor unit architecture refers to its:
size, distribution and endplate area
Which type of motor units fire first?
Type I, smallest
In EMG the needle is the ____ electrode
active
The reference for EMG should be placed
over the muscle being tested
The ground for EMG can be placed
anywhere on the extremity being tested
A monopolar needle records the voltage differences between
the needle tip and the reference electrode
Which registers a larger potential - a monopolar or concentric needle?
monopolar
A monopolar needle electrode picks up from a ____ degree field
360
A concentric needle electrode picks up from a ____ degree field
180
Which registers more polyphasicity- a monopolar or concentric needle?
monopolar
4 parts to the EMG
1. insertional activity
2. muscle at rest
3. analyze motor unit
4. recruitment
Basic filter and amplifier settings to check prior to starting EMG
- low freq filter 10-30 Hz
- high filter 10,000-20,000 Hz
- amplifier sensitivity 50-100 microvolts per division
- sweep 10ms per division
Inserting a needle into atrophied muscle often feels like inserting the needle into
sand
Insertional activity that lasts longer than ____ ms is considered increased
300
List 4 examples of spontaneous activity generated by muscle
- fibrillation potentials
- positive sharp wave
- myotonic discharges
- complex repetitive discharges
List 6 examples of spontaneous activity generated by nerve
- myokymic discharges
- cramps
- neuromyotonic discharges
- tremors
- multiples
- fasciluations (may be mm or nerve)
Gain on EMG for looking at sponateous activity often needs to be set at
50-100microvolts
7 examples of chronic muscle disorders associated with positive sharp waves and fibrillation potentials
- inflammatory myopathies
- muscular dystrophies
- inclusion body myositis
- cogenital myopathies
- rhabdomyolysis
- muscle trauma
- trichinosis
6 examples of neurogenic disorders associate with positive sharp waves and fibrillation potentials
- radiculopathy
- axonal peripheral neuropathy
- plexopathies
- entrapment neuropathies
- motor neuron disease
- mononeuropathies
5 examples of chronic muscle disorders associated with complex repetitive discharges
- myopathies
- inflammatory processes
- limb-girdle dystrophy
- myxedema
- Schwartz-Jampel syndrome
5 examples of neurogenic disorders associated with complex repetitive discharges
- chronic myopathy or radiculopathy
- poliomyelitis
- spinal muscular atrophy
- motor neuron disease
- hereditary neuropathies
Complex repetitive discharges are suggestive that the lesion is more than ____ old.
6 months
Clinical correlation of myotonic discharges on EMG
delayed muscle relaxation after a forceful contraction
7 examples of disorders associated with myotonic discharges
- myotonic dystrophy
- myotonia congenita
- paramyotonia
- hyperkalemic periodic paralysis
- polymyositis
- acid maltase deficiency
- chronic radiculopathy/neuropathy
5 examples of disorders associated with myokymic discharges
Facial muscles:
- Bell's palsy
- multiple sclerosis
- polyradiculopathy
Limbs:
- chronic nerve lesions
- radiation plexopathy
3 things that tell you you are likely in the endplate region
1. Miniature endplate potentials
2. Endplate spikes
3. Pain
MEPPs represent
spontaneous release of Ach from the presynaptic terminal and the resultant local depolarization
Endplate spikes represent
single muscle fiber depolarizations
What do positive waves mean when they are found in the endplate?
They are likely a normal finding and interpretation otherwise is not wise
What should you do if you find yourself in the endplate?
Get out; either by withdrawing needle or advancing firmly
Typical sweep speed and gain during minimal contraction during EMG?
sweep 10msec/div
gain 200-500 microvolts
4 parameters to evaluate the components of motor unit action potential morphology
1. amplitude
2. rise time
3. duration
4. phases
MUAP amplitude is measured from
most positive to most negative peak
Acceptable rise time on MUAP is ___msec or less
0.5
Duration is measured as
the initial departure from baseline to the return to baseline
Normal MUAP duration (general)
5-15 msec
Why is MUAP duration often decreased in myopathies?
Because there are fewer muscle fibers available to contribute to the MUAP.
2 major ways of counting phases:
1. the number of times it crosses the basline
2. the peaks and valleys across baseline +1
Which is a better measure of pathology, motor unit duration or polyphasicity?
duration
Name the two ways that a muscle contraction can become stronger
1. the same motor unit fires faster
2. additional motor units fire
The INITIAL motor unit firing (patient just thinking about moving the muscle) is often
2-3 Hz and irregular; switches to regular when at 5 Hz
How do you find the recruitment ratio?
Hz of fastest motor unit divided by the number of motor units
MUAP recruitment ratio above 8 suggests
neuropathic process
MUAP recruitment ratio less than 3 suggests a
myopathic process
Why is it difficult to evaluate type II motor fibers on EMG?
By the time type II fibers are recruited the baseline is obscured by the activity of type I fibers
Why might EMG be normal in a patient with a steroid myopathy?
Steroid myopathy typically involves type II fibers which are not easily studied on EMG
What are the three types of nerve injury in the Seddon classification of nerve injuries?
- neurapraxia
- axonotmesis
- neurotmesis
What is neurapraxia?
Damage to the myelin
Damage to myelin is called
neurapraxia
What is axonotmesis
injury only affecting the nerve's axons
An injury only affecting the nerve's axons is called
axonotmesis
What is neurotmesis?
injury affects the myelin, axons and all supporting structures
injury that affects the myelin, axons and all supporting structures is labeled
neurotmesis
Name the 4 general categories of demyelinating injuries
1. uniform demyelination
2. segmental demyelination
3. focal nerve slowing
4. conduction block
Where is uniform demyelination typically seen?
in hereditary disorders such as Charcot-Marie-Tooth disease
Clinically, conduction block should present as
weakness
In a pure neurapraxia, EMG testing will be
normal (unless conduction block is present)
What would EMG show if there is conduction block?
decreased recruitment
How fast do peripheral nerve axons regrow?
1mm/day, 1 inch per month
Effect of cold temp on latency
prolonged (0.2 ms/degree C)
Effect of cold on amplitude
increased (sensory more than motor)
Effect of cold on conduction velocity
decreased (1.8-2.4 m/s/degree C)
Effect of cold on duration
increased
Repetitive nerve stimulation in a patient with NMJ disease is likely to be _____ if they are cold
normal
General temperature goals in NCS
- upper limb: above 32C
- lower limb: above 30C
Positive initial deflection in CMAP with median nerve stimulation at the wrist should prompt consideration of
Martin-Gruber Anastomosis
Why may an EMG study appear normal when a radiculopathy likely exists?
[1] Lesion is too Acute (<3 weeks). [2] The nerve root is compressed with demyelination without axonal loss. [3] If only the sensory nerve root is affected. [4] Some sampled fascicles may be preferentially spared, thus appearing normal (important to sample several areas of the muscle-Quadrants). [5] Paraspinal muscles may have already re-innervated.
On NCV, axonal loss may be suspected when you see this.
Decreased amplitude with either normal or slightly slowed conduction velocity and distal latency
Concentric needle?
Contains both the active and reference electrodes
Monopolar needle
Only contains the active electrode
When inserting the needle, what two things should be evaluated?
Insertional activity and spontaneous activity
Define abnormal insertional activity
Any activity other than endplate potentials lasting longer than 300ms after brief needle movement and/or none
Define spontaneous activity
Any activity at rest lasting longer than 3 seconds
The usual settings for EMG insertion are sweep speed at ___ ms per division and sensitivity at ___ microvolts per division.
10 ms and 50 microvolts
In EMG, when evaluating MUAP's, the setting are: sweep speed at ___ ms per division and sensitivity at ___ microvolts per division.
10 ms and 200 microvolts
True or False. During needle EMG, it is important to locate a sharp or crisp MUAP prior to accessing activation and recruitment
True. This allows for the highest amplitude and shortest duration to be recorded
During a needle EMG, along with activation and recruitment, what three major things are being evaluated?
Duration, amplitude and number of phases
Miniature endplate potentials are seen when the needle is inserted into an _____
Neuromuscular Junction (NMJ) or endplate zone heard as endplate noise
A negative peak followed by a short positive peak is called a _____ potential.
Biphasic
True or False. Biphasic potentials are a normal finding.
True. They are seen when terminal nerve twigs are irritated during needle insertion. "Endplate Spike" is a MFAP
A MFAP that begins with an initial positive deflection are known as (2 names)
Positive Sharp Waves and Fibrillation Potentials
Positive Sharp Waves and/or Fibrillation Potentials suggest what basic pathology?
Denervation
Miniature Endplate Potentials (MEPP), Muscle Fiber (PSW-FIBS), Multiple Muscle Fibers and Motor Unit Action Potentials (MUAP) describe the ______ of a spontaneous discharge.
Morphology. The morphology (amplitude, duration and # of phases) helps to define the specific source generator
MUAP stands for Motor Unit Action Potential and is defined as.....
Spontaneous discharges generated by the motor neuron or its axon. Included are fasciculations, tetany, myokymic discharges, neuromyotonic discharges, cramps and resting tremors.
A normal MUAP has typically (number of) phases, and has a duration of (? ms) and has variable amplitude.
2-4 phases and 5-15ms in duration
What would be the best way to differentiate a MFAP from a MUAP?
A MFAP has a much smaller duration and amplitude compared with a MUAP
MFAP's that wax and wane are associated with what type of discharge?
Myotonic
Neuromyotonic discharges are noted by what characteristic finding
A marked decrementing of MUAP amplitude as in a "pinging" sound
Complex repetitive discharges typically are stable but may change abruptly due to . . . .
a drop out or sudden change in loops or circuits
What is the typical sound associated with endplate noise
a seashell sound
A Fibrillation Potential is the spontaneous firing of a
single muscle fiber
A 'rain on the roof' sound is associated with these potentials
Fibrillations, recognized by their single MFAP morphology: brief initial positive spike, 1-5ms duration and low amplitude (10-100 microvolts) and regular firing pattern 0.5 to 10 Hz
T or F. A positive sharp wave differs from a fibrillation potential in that they sound more like a 'pop' than rain on the roof
True. They also have similar amplitudes and rates and are signs of active denervation
Complex Repetitive Discharges are the result of .....
depolarization of a single muscle fiber followed by ephaptic spread to adjacent denervated fibers creating a circus movement whereby the original depolarized fibers act as the pacemaker for the loop
A Myotonic discharge has a characteristic sound pattern described as
waxing and waning of amplitude and frequency. Revving engine sound.
T or F. A reinnervated motor unit may present as a large fasciculation
True. The usual origin has been the anterior horn cell, but recent studies have placed the origin in the distal axon.
What are the clinical signs that help differentiate a benign vs. pathologic fasciculation?
In benign fasciculations, you would likely not have muscle weakness, atrophy or abnormal reflexes
What is the typical sound and rate of a fasciculation?
Like "corn popping" in dull sounding irregular patterns
How are Endplate spikes are different from fibrillation potentials?
The irregular rate / sound is sputtering, cracking or buzzing vs. regular rate, rain on the roof. They also have an initial negative deflection
Normal spontaneous activity as seen often in EMG studies include
Insertional activity, endplate noise (miniature end plate potentials) and endplate spikes
Abnormal Muscle Fiber Potentials include:
Fibrillation Potentials, Positive Sharp Waves, Complex Repetitive Discharges and Myotonic Discharges
Abnormal Motor Unit Potentials include:
Fasciculation Potentials, Doublets, Triplets and Multiplets, Myokymic Discharges, Cramps, Neuromyotonic Discharges and Rest Tremors
Positive waves and Fibrillation potentials both represent what?
Spontaneous depolarization of a muscle fiber
Biceps Femoris (Short Head)
Peroneal division /Sciatic N. / Lumbosacral Plexus / L5-S1-S2 (S1)
The only Peroneal N. supplied muscle above the Knee
Biceps Femoris (Short Head)
Gluteus Maximus is supplied by what nerve?
Inferior Gluteal Nerve / L5-S1-S2 (S1)
Gluteus Medius is supplied by what nerve?
Superior Gluteal Nerve / L4-L5-S1 (L5)
Gluteus Minimus is supplied by what nerve?
Superior Gluteal Nerve / L4-L5-S1 (L5)
Rectus Femoris Nerve & Root?
Femoral Nerve / Lumbar Plexus / L2-3-4 (L2-3)
Iliopsoas: Nerve & Root?
Femoral Nerve / Lumbar Plexus / L2-3-4 (L2-3)
Tensor Fasciae Latae: Nerve & Root?
Superior Gluteal Nerve / L4-L5-S1 (L5)
Vastus Medialis: Nerve & Root?
Femoral Nerve / Lumbar Plexus / L2-L3-L4 (L3-4)
Vastus Lateralis: Nerve & Root?
Femoral Nerve / Lumbar Plexus / L2-L3-L4 (L3-4)
Adductor Longus: Nerve & Root?
Obturator Nerve / Lumbar Plexus / L2-L3-L4 (L3)
Semimembranosus: Nerve & Root?
Tibial Division / Sciatic N. / Lumbosacral Plexus / L4-L5-S1 (L5)
Semitendinosus: Nerve & Root?
Tibial Division / Sciatic N. / Lumbosacral Plexus / L4-L5-S1 (L5)
Adductor Digiti Quinti Pedis: Nerve & Root?
Lateral Plantar Nerve / Tibial N. / Sciatic N. / Lumbosacral Plexus / S1-S2 (S1)
Adductor Hallucis Brevis: Nerve & Root
Medial Plantar N. / Tibial N. / Sciatic N. / Lumbosacral Plexus / S1-S2 (S1)
Gastrocnemius-Medial Head: Nerve & Root
Tibial N. / Sciatic N. / Lumbosacral Plexus / S1-S2 (S1)
Tibialis Posterior: Nerve & Root
Tibial N. / Sciatic N. / Lumbosacral Plexus / L5-S1 (L5)
Flexor Digitorum Longus: Nerve & Root
Tibial N. / Sciatic N. / Lumbosacral Plexus / L5-S1 (L5)
Peroneus Longus: Nerve & Root
Superficial Peroneal N. / Common Peroneal N. / Sciatic N. / Lumbosacral Plexus / L5-S1 (L5)
Tibialis Anterior: Nerve & Root
Deep Peroneal N. / Common Peroneal N. / Sciatic N. / Lumbosacral Plexus / L4-L5
Extensor Digitorum Longus: Nerve & Root
Deep Peroneal N. / Common Peroneal N. / Sciatic N. / Lumbosacral Plexus / L4-L5 (L5)
Extensor Hallucis Longus: Nerve & Root
Deep Peroneal N. / Common Peroneal N. / Sciatic N. / Lumbosacral Plexus / L4-L5-S1 (L5)
Extensor Digitorum Brevis (EDB): Nerve & Root
Deep Peroneal N. / Common Peroneal N. / Sciatic N. / Lumbosacral Plexus / L4-L5-S1 (L5)
Important muscle to sample in suspected lesions of the peroneal nerve at the fibular neck.
Biceps Femoris - Short Head L5-S1-S2 (S1)
This muscle will help differentiate lesions of the lumbar plexus or lumbar roots from femoral neuropathy.
Adductor Longus L2-3-4 (L3)
Name an S1 innervated muscle on the medial side of the foot & the Nerve innervation
Adductor Hallucis Brevis / Medial Plantar N. / Tibial N. / Sciatic N. / Lumbosacral Plexus/S1
When Footdrop is present, this muscle is useful to sample to differentiate from a Peroneal neuropathy.
Tibialis Posterior is a primarily L5 innervated muscle that is supplied by the Tibial Nerve
The EDB is a distal muscle that is supplied by what nerve?
Deep Peroneal N. / L5
The Extensor Hallucis Longus has strong innervation by what Root Level?
L5, by way of the Deep Peroneal N. / Common Peroneal N. / Sciatic / LS Plexus
In a pure compressive lesion at the fibular neck, would you suspect a sensory loss over the lateral aspect of the knee?
No. The take off of the Lateral Cutaneous N. of the Knee is above the fibular neck
The primary evertor of the ankle is what muscle and what is it's nerve supply?
Peroneus Longus/brevis innervated by the Superficial Peroneal N.
What weakness might you see in an L3 Femoral Root lesion?
Knee Extension / Hip Flexion / Leg Adduction
If ankle inversion is noted weak, what nerve may be involved?
Tibial N. innervates the Tibialis Posterior
Sensory innervation of the medial leg is derived from this nerve and root level.
Saphenous N. / Femoral N. / L2-L3-L4
Sensory innervation of the lower posterior leg and lateral foot is derived from this nerve.
Sural N., Formed from the Medial Sural Cutaneous N. (Tibial) and Lateral Sural Cutaneous N. (Peroneal)
The medial thigh sensory is primarily derived from these nerves
Medial and Intermediate Cutaneous Nerves of the Thigh / Femoral / L2-3-4.
The Lateral Thigh obtains it's sensory via the ________ Nerve. What Root Level?
Lateral Cutaneous Nerve of the Thigh / L2-3
Meralgia Paresthetica involves what nerve? Likely cause?
Lateral Cutaneous Nerve of the Thigh / L2-3. Entrapment under the Inguinal ligament (obese, tight clothes/underwear, diabetes)
What is an electromyograph?
Measures our voltage (compound muscle action potential--CAMP)
What is CMAP also known as?
M-wave
What is a compound muscle action potential (CAMP)?
Temporal and spatial summation of muscle fire action potentials in a given volume
What is a differential amplifier?
Amplifies the difference in voltage between 2 recording electrodes (need to amplify due to our small voltages)
Why must our voltage be amplified when recording muscle APs?
The voltages in our system are very small relative to ambient noise, so amplifying the difference allows detection of very small voltages
What happens when the voltage is the same under each electrode (half between in distance)?
When the noise is the same under each electrode and we amplify, the noise will cancel out
Recording the CMAP is recording a
single muscle fiber
As CAMP propagates, it will sequentially
alter the voltages under the recording electrodes
What will influence the CMAP recording?
differences and changes in conduction velocity will influence the recording
What must you take into account when recording CMAPs and seeing the m-waves spreading out?
Fatigue in the muscle due to decrease in velocity
Fixed distance of electrodes
Surface electrodes that will pick up several muscle fibers (nerve conduction velocity measuring distance over time)
Needle electrodes are used to
measure single action potential and motor unit (can't get this info with surface electrodes)
What type of EMG is easy to use and also misuse?
Surface EMG
Place electrodes for surface EMG
parallel to muscle orientation and over the midbelly of muscle (where superficial nerve is)
How EMG signal processed in order to be read after recording?
Goes from raw to rectified (absolute value) by averaging the amplitude
What must you synch the EMG with?
Force signal along with a machine that will record time
To get a single twitch, you must increase
stim amplitude until m-wave plateaus (force will increase by recruiting more motor units)
To get train of action potentials (rate coding), set amplitude with
twitch and increase frequency for force; the m-wave amplitude should not change
To measure volitional activity, rather than using stim's force frequency setup have the patient
contract their muscle
With volitional isometric contraction, what kind of relationship is there?
Fairly strong linear relationship between force and EMG, not perfect with some issues of amplitude cancellation because some motor neurons are firing at different times
With movement, the force EMG (velocity) relationship no longer holds, why?
Only holds true because when we move, the moment arm is constantly moving with length-tension curve changes allowing force to change constantly
What is kinesiological EMG mostly used for?
Mostly for timing of muscle activation and is used for research applications, gait labs
What does EMG biofeedback promote?
Muscle activation and relaxation
What is diagnostic EMG?
Requires invasive needles/wires (very different from kinesiological EMG)
What other test is often done with diagnostic EMG?
Nerve conduction velocity studies (NCV)
What other test is often done with nerve conduction velocity studies?
Diagnostic EMG
What does nerve conduction velocity studies measure?
the impulse propagation in peripheral sensory or motor nerve (speed of APs)
Electromechanical delay
The time between the onset of the m-wave and the onset of the force
H-reflex testing
An electrically-elicited stretch reflex
H-reflex is often observable at
low intensity stimulation
H-reflex tends to decline with
an increase in intensity (bigger m-wave)
Why does the H-reflex diminish when increasing the intensity (bigger m-wave)
Antidromic signal from the e-stim cancels out the H-reflex
What reasons may you want to do H-reflex testing?
UMN lesions with hyperexcitable reflexes or those with high tone (big H-reflex) or low tone (small H-reflex)
Stimulus artifact
initial downward spike from the electrodes picking up the high voltage pulse coming out of the stimulator because we are good conductors
Other biofeedback mechanisms aside from EMG
Heart or respiratory rate
Skin impedance
Blood pressure
Temperature
Positional (neutral spine)
EMG processing is similar to
kinesiology
Raw EMG is converted to an when using EMG biofeedback
envelope
What types of feedback are scaled relative to the patient's response with EMG biofeedback
Series of light bars and audio tones
How would you set the level to promote muscle activation with EMG biofeedback?
Set level higher than what already have
What sort of feedback would you use to promote muscle activation with EMG biofeedback?
Use light or audio to turn on noise if patient enjoys it or turn off noise if it is irritating
How would you set the level to promote muscle relaxation with EMG biofeedback?
Set level lower than what they are already contracting at (show them with different muscle what it is supposed to measure, then place electrodes over their area to show them the tension)
What sort of feedback would you use to promote muscle relaxation with EMG biofeedback?
Audio set to turn off (if on, may alarm them)
What are diagnostic EMG/NCV studies used for?
Identifying neuromuscular impairments (peripheral nerve injuries, myopathies, etc)
Testing of diagnostic EMG/NCV is based on
peripheral phenomena
What are often inferred from peripheral observations when doing diagnostic EMG/NCV tests?
Central phenomena, which is not always accurate
Neuropraxic
damage to the myelin (local demyelination)
Axonotmetic
damage to myelin and axon, but sheath in tact
Neurotmetic
damage to myeline, axon and sheath (denervated changes and won't regenerate)
Insertional activity when diagnostic needle EMG testing
normally quite brief when needle penetrates the membrane (300 milliseconds)
Prolonged insertional activity with diagnostic EMG
Greater than 300 to 500 milliseconds (hyperexcitable membrane that typically indicated denervated muscle or muscle inflammation)
What indicates denervation of a muscle with diagnostic EMG?
Prolonged insertional activity, positive sharp waves and fibrillation potentials
How could you discriminate denervation and muscle inflammation if results from diagnostic EMG showed prolong insertional activity?
Ask patient to contract their muscle voluntarily; if can do so then muscle inflammation
Reduced insertional activity with diagnostic EMG
Less than 100 milliseconds indicating a lost of fibers (severe atrophy or muscle necrosis/fibrosis)
What is the muscle activity like after inserting a needle into the membrane with diagnostic EMG?
Brief activity of 300 to 500 milliseconds and the no activity
Spontaneous activity after insertional diagnostic EMG
Positive sharp waves (sawtooth)
Fibrillation potentials
What indicates severe atrophy or muscle necrosis/fibrosis (loss of fibers) with a diagnostic EMG?
Reduced insertional activity of less than 100 milliseconds
Positive sharp waves (sawtooth) parameters
50 to 100 per second (0.01 to 1 millivolt)
Positive sharp waves (sawtooth) indicates
denervation of muscle, demyelination or local muscle trauma
Fibrillation potentials parameters
Biphasic 1 to 30 per second (20 to 2000 microvolts)
Fibrillation potentials associated with
denervation (increase spread of ACHRs)
What is the difference between fibrillation potentials and positive sharp waves?
Fibrillation potentials may differ due to tissue filtering (signal further away)
Complete interference pattern
Muscle contraction activity with no baseline being shown in diagnostic EMG
Incomplete interference pattern
Muscle contraction activity when baseline is seen indicating atrophy, muscle injury or partial denervation (not all fibers are recruited)
With peripheral nerve injury, often need to wait how many days to see abnormal potentials to appear using diagnostic/NCV tests? Why?
10 days because depending on where the injury occurred, it will take awhile for the nerve to die off
What kind of electrodes can you use when using NCV/EMG testing?
Surface or needle electrodes
For motor nerve, what do you assess when using NCV/EMG testing?
Compound muscle action potential (CMAP)
How long after injury must wait to do NCV/EMG tests?
A week or more after injury (if acute) to allow for better discrimination
Diagnostic EMG can help estimate
acuity of the condition
After 10 days of injury, can still see m-wave would indicate what possible injury with NCV/EMG tests?
Complete neuropraxia (myelin disrupted)
After 10 days of injury, m-wave is no longer present with NCV/EMG testing
Complete axonotmesis (myelin and axon damaged or died off) or complete neurotmesis (myelin, axon and sheath are damaged)
After 10 days of injury, m-wave is smaller compared to 1st day indicates what with NCV/EMG testing
Incomplete mixed lesion (partial denervation)
What is the key to NCV/EMG testing?
You have to wait 10 days to discriminate m-waves
Where can you calculate latency when using NCV?
from stimulation at 2 sites and measure the distance between
NCV =
conduction distance divided by proximal latency minus distal latency
What assumptions are there when calculating NCV?
Assumes that we have a linear course of nerve paths (nerves run in a straight line)
Latency
From the time of the stimulus artifact to the onset of the m-wave (CMAP)
Nerve conduction velocity studies show
latencies and conduction blocks
What is used to determine nerve conduction
Latency
Sensory NCV measures
compound nerve action potential (CNAP) or compound sensory nerve action potential (CSNAP)
CNAP is often what compared to CMAP?
smaller (especially with surface electrodes)
What does CNAP require more of compared to CMAP? Why?
Signal averaging (taking repetitive measurements) in order to cancel out noises
How is CNAP typically performed?
By stimulating the digits
Why is CNAP typically stimulated at the digits?
Place with lots of sensory nerves and no muscle to activate
CNAP is done typically with how many latencies? Why?
1 verses 2 with motor NVC...not sure why?
Calculating motor latencies can also reveal with NCV
conduction blocks
Smaller m-wave located at axilla compared to above the elbow
Nerve block located somewhere between axilla and above the elbow
What may be the problem with measuring NVC in diabetics
Both sides would be impaired since diabetes is a systemic problem; typically we would measure both sides with NCV if there is a unilateral problem
Standard NCV norms for motor upper extremity
45 to 70 m/s
Standard NCV norms for motor lower extremity
60 m/s
Standard NCV norms for sensory upper extremity
50 to 75 m/s
Standard NCV norms for sensory lower extremity
60 m/s
NCV values reflect the conduction velocity of the
fastest conducting neurons stimulated (could have small slower axon conduction and not be shown on NCV test--this is very limiting!)
Deltoid
C5/6 - axillary
biceps
C5-6 musculoculateous
pronator teres
c6-7 median
EDC
C7 PIN/Radial
Triceps
C7 radial
FCU
C8 ulnar
FCR
C7 median
APB
C8/T1 median
FDI
C8/T1 ulnar
Infraspinatus
C5/6 suprascapular
EI
C7/8 radial
ADM
C8/T1 ulnar
Adductor longus
L3 obturator
vastus medialis
L3 femoral
rectus femoris
L3 femoral
ant tib
L4/5 deep fibular
post tib
L5/S1 tibial
Short head biceps fem
L5/S1 fibular portion of siatic
TFL
L5 superior gluteal
Med gastroc
S1 Tibial
lat gastroc
S1 tibial
Ext hallucis
L5 deep fibular
Peron longus
L5/S1 superficial fibular
Adductor hallucis
S1/2 medial plantar /tibial
FDI peron
S1/2 lateral plantar/ tibial
Glut medius
L5 superior gluteal
glut max
S1 inf gluteal
muscles innnervated by the PIN
■Extensor carpi ulnaris
■Extensor digitorum
■Extensor digiti minimi
■Abductor pollicis longus
■Extensor pollicis longus
■Extensor pollicis brevis
■Extensor indicis proprius (most distal)
Muscles in dorsal forearm NOT innervated by PIN
the PIN innervates all the muscles on the dorsal side of the forearm, EXCEPT the brachioradialis, extensor carpi radialis longus (ECRL), and anconeus.
AIN
- arises from median nerve, 5 cm above medial epicondyle;
- runs on volar surface of FDP and along interosseous membrane between ulna & radius;
- supplies FPL, lateral half of FDP, & pronator quadratus;
- Primarily motor
C3 dermatome
clavicle
C5 dermatome
Lateral arm above elbow
C4 dermatome
Over shoulder tip
C6 dermatome
Lateral forearm down to thumb. Both palmar and dorsal thumb
C7 dermatome
Tip of index finger, palmar surface.
C8 dermatome
Dorsal surface of pinkie.
T1 dermatome
Medial anterior forearm in cubital fossa.
T2 dermatome
T2: Medial armpit.
L1 dermatome
L1: groin, hands in pockets. Inguinal Ligament IL LI.
L2 dermatome
L2: groin, at sapheno femoral junction, 4 cm below and lateral to pubic tubercle
L3 dermatome
L3: Medial thigh.
L4 dermatome
L4: Medial lower leg.
L5 dermatome
L5: Cleft between first digit and second. Lateral lower leg.
S1 dermatome
S1: Lateral malleolus. Sole.
S2 dermatome
S2: Medial back of leg, medial behind knee.
S3,4, 5
S3,4,5: Saddle.