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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 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.
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).
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 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.
What are the 7 components of the motor unit (from proximal to distal)?
- anterior horn cell
- nerve root
- spinal nerve
- 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
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
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 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
Beta motor neurons innervate _____
intrafusal and extrafusal fibers (skeletal muscle and the muscle spindle)
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.
Connective tissue surrounding bundles or fascicles of myelinated and unmyelinated nerve fibers
loose connective tissue surrounding the entire nerve that holds the fascicles together and protects it from compression
What are "leak channels"?
Channels that allow K and Na to move passively in and out of the cell membrane
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?
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
action potential is monitored traveling in the direction of its typical physiology conduction (usually described as away or toward the spinal cord)
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 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?
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
What are "presynaptic active zones" in the motor neuron?
Areas on the presynaptic membrane where acetylcholine is released
During the periods of inactivation in a motor unit, a spontaneous release of Ach quanta occurs every __ seconds
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?
Normally, the end-plate potential amplitude is ___ times amount needed to initiate an action potential
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)
How can the muscle fiber depolarization penetrate deeper into the muscle?
T-tubule system (calcium is released from the sarcoplasmic reticulum)
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?
- 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
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
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
6 sources of environmental electrical noise interference in EMG/NCS
- EMG audio feedback
- needle artifact
- 60Hz interference
- fluorescent lights
- the patient
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 does the common mode rejection ratio tell you?
The larger the CMRR the more efficient the amplifier
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 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
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
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
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
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)
Define latency of activation
The time between initiation of the electical stimulus and the beginning of saltatory conduction
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)
Why is there so much amplitude drop with proximal SNAP stimultion?
Phase cancellation; more pronounced with short duration 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)
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
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 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 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?
- 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 is the general pathway for an f-wave?
antidromic motor to the spinal cord with orthrodromic motor return
Is the f-wave latency constant or variable? why?
variable. It's a polysynaptic response where renshaw cells can have an inhibitory effect
Limitations of the f-wave
- evaluates a long pathway which can dilute focal lesions
- only assess motor fibers
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 is affected by lesions of the...
- trigeminal nerve
- 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
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
- middle ear infections
- 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)
Trace the ascending pathway for SSEPs
peripheral nerve --> plexus --> root --> spinal cord (posterior column)--> contralateral medial lemniscus --> thalamus --> somatosensory cortex
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
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
2 main causes of increased insertional activity on needle EMG
- irritable cell membrane
4 main causes of decreased insertional activity on needle EMG
- electrolyte abnormalities
Describe the appearance of MEPPs on needle EMG
10-50uV non-propagated potential - generally appears as an irregular baseline
What is the underlying pathophysiology of a fibrillation?
denervated single muscle fibers from uncontrolled ACh release
Why don't positive sharp waves have a negative phase?
because they are propagated to but not beyond the needle tip
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
Classic causes of CRDs
- anterior horn cell diseases
- chronic radiculopathy
- peripheral neuropathy
- musclar dystrophy
- limb girdle dystrophy
* can be normal variant
Classic diseases where myotonic discharges are found
- chronic radiculopathy
- peripheral neuropathy
- myotonic dystrophy
- myotonia congenita
- maltase deficiency
- hyperkalemic periodic parlysis
Typical causes of myokymia in the extremities
radiation plexopathy, compression neuropathy, rattlesnake venom
Why do neuromyotonic discharges taper off at the end?
because the single muscle fiber firing fatigues
Causes of cramp discharge on EMG
- salt depletion
- 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)
When are doublet/multiplet potentials seen?
- motor neuron diseases
- metabolic diseases
Describe "early recruitment" on EMG
many motor units start firing early with activation (hard to fire just one unit)
What is the recruitment frequency?
The firing rate of the first motor unit when the second unit starts to fire
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 an interference pattern on EMG?
the electrical activity recorded from a muscle during maximum voluntary contraction
4 major uses for electrodiagnostics (reasons to order)
3. help determine treatment
Role of filters (most generally)
faithfully reproduce the signal you want while trying to exclude both high and low frequency electrical noise
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
How can you verify that a low amplitude is from segmental demylination and resultant temporal dispersion?
the area under the curve should be unchanged
What facilitates the H-reflex?
* anything that increases motor-neuron pool excitability (contraction, CNS lesion)
3 major uses of the F-wave
Proximal nerve/root injury
Reproducibility of the H-reflex
latency and configuration reproducible, amplitude varies depending on stimulation
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)
A monopolar needle records the voltage differences between
the needle tip and the reference electrode
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
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
- neuromyotonic discharges
- fasciluations (may be mm or nerve)
7 examples of chronic muscle disorders associated with positive sharp waves and fibrillation potentials
- inflammatory myopathies
- muscular dystrophies
- inclusion body myositis
- cogenital myopathies
- muscle trauma
6 examples of neurogenic disorders associate with positive sharp waves and fibrillation potentials
- axonal peripheral neuropathy
- entrapment neuropathies
- motor neuron disease
5 examples of chronic muscle disorders associated with complex repetitive discharges
- inflammatory processes
- limb-girdle dystrophy
- Schwartz-Jampel syndrome
5 examples of neurogenic disorders associated with complex repetitive discharges
- chronic myopathy or radiculopathy
- spinal muscular atrophy
- motor neuron disease
- hereditary neuropathies
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
- hyperkalemic periodic paralysis
- acid maltase deficiency
- chronic radiculopathy/neuropathy
5 examples of disorders associated with myokymic discharges
- Bell's palsy
- multiple sclerosis
- chronic nerve lesions
- radiation plexopathy
3 things that tell you you are likely in the endplate region
1. Miniature endplate potentials
2. Endplate spikes
spontaneous release of Ach from the presynaptic terminal and the resultant local depolarization
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?
gain 200-500 microvolts
4 parameters to evaluate the components of motor unit action potential morphology
2. rise time
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
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
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?
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
Repetitive nerve stimulation in a patient with NMJ disease is likely to be _____ if they are cold
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
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
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
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
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
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
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
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)
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 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 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
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)
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
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 nerve conduction velocity studies measure?
the impulse propagation in peripheral sensory or motor nerve (speed of APs)
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)
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
Positional (neutral spine)
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)
What are often inferred from peripheral observations when doing diagnostic EMG/NCV tests?
Central phenomena, which is not always accurate
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)
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) indicates
denervation of muscle, demyelination or local muscle trauma
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
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
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)
Where can you calculate latency when using NCV?
from stimulation at 2 sites and measure the distance between
What assumptions are there when calculating NCV?
Assumes that we have a linear course of nerve paths (nerves run in a straight line)
Sensory NCV measures
compound nerve action potential (CNAP) or compound sensory nerve action potential (CSNAP)
What does CNAP require more of compared to CMAP? Why?
Signal averaging (taking repetitive measurements) in order to cancel out noises
Why is CNAP typically stimulated at the digits?
Place with lots of sensory nerves and no muscle to activate
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
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!)
muscles innnervated by the PIN
■Extensor carpi ulnaris
■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.
- 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
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