Why can normal proximal sensory studies have decreased amplitude?
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?
What is the longest latency when compared to the upper limit of normal that a normally myelinated nerve can have? Hint %.
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?
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)?
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?
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
Connective tissue surrounding each individual axon and its myelin sheath
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?
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
Most important event in generating an action potential is...
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?
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
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
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
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
Location of the dorsal root ganglion
In the neural foramen
Which is more sensitive in detecting an incomplete peripheral nerve injury, SNAPs or CMAPs?
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
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 ______
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?
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
in hereditary disorders such as Charcot-Marie-Tooth disease
Clinically, conduction block should present as
In a pure neurapraxia, EMG testing will be
normal (unless conduction block is present)
What would EMG show if there is conduction block?
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
Repetitive nerve stimulation in a patient with NMJ disease is likely to be _____ if they are cold
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
Why may an EMG study appear normal when a radiculopathy likely exists?
 Lesion is too Acute (<3 weeks).  The nerve root is compressed with demyelination without axonal loss.  If only the sensory nerve root is affected.  Some sampled fascicles may be preferentially spared, thus appearing normal (important to sample several areas of the muscle-Quadrants).  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
Contains both the active and reference electrodes
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.
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?
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?
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
the PIN innervates all the muscles on the dorsal side of the forearm, EXCEPT the brachioradialis, extensor carpi radialis longus (ECRL), and anconeus.
- 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
Lateral arm above elbow
Over shoulder tip
Lateral forearm down to thumb. Both palmar and dorsal thumb
Tip of index finger, palmar surface.
Dorsal surface of pinkie.
Medial anterior forearm in cubital fossa.
T2: Medial armpit.
L1: groin, hands in pockets. Inguinal Ligament IL LI.
L2: groin, at sapheno femoral junction, 4 cm below and lateral to pubic tubercle
L3: Medial thigh.
L4: Medial lower leg.
L5: Cleft between first digit and second. Lateral lower leg.