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275 Cards in this Set

  • Front
  • Back
For neuronal injury, what is considered "brief" ischemia
6 hours or less
General pathologic changes that occur in nerve with brief ischemia
- no structural changes to nerve
- may be surrounding edema
Which fibers are most effected by crush/tourniquet injury?
larger fibers more than smaller
Complete conduction block occurs when internodal conduction times exceed _____
500-600 microseconds
Why does significant demyelination result in complete conduction block instead of just severe slowing?
sodium channels are focused at nodes of Ranvier and not available along the section of demyelinated axon
Pathological changes in muscle after neurapraxic lesions
- few direct changes
- may have disuse atrophy if more prolonged
Axonal changes in axonotmesis at 2 days, 3 days and 8 days after injury
2 days:
- leakage of intra-axonal fluid from severed nerve
- swelling of distal nerve segment
- disapearance of neurofibrils in the distal segment

3 days:
- fragmentation of axon and myelin
- digestion of myeline components

Day 8:
- axon digested
- Schwann cells attempt to bridge the gap between 2 segments
Cell body changes in axonotmesis at 48 hours and 2-3 weeks
48 hours:
- Nissl bodies break apart

2-3 weeks:
- nucleus and nucleolus displaced eccentrically
What is the ideal timing for electrodiagnostic studies after peripheral nerve trauma?
- 3-4 weeks in general (fibrillations apparent on EMG)
- at 7-10 days may be able to differentiate conduction block from axonotmesis
- 2 months post injury if lesion documented surgically and EMG is just to document recovery
Changes in CMAP in neurapraxic lesions immediately after injury
normal distal to site of lesion and smaller/absent CMAP proximal to the lesion
When evaluating CMAP along a peripheral nerve, what change in amplitude with distance would be clearly abnormal?
greater than 20% drop over 25cm or less
Give 2 reasons for slowing in a neurapraxic lesion
- loss of fast conducting fibers
- demylintion of surviving fibers
Changes in CMAP in neurapraxic lesions should resolve within what time frame
a couple of months
How do traumatic peripheral nerve lesions with axonotmesis look different on electrodiagnostics than on those with neurotmesis?
they look the same because differences are in the surrounding tissue
Changes in CMAP within the first few days of a nerve injury with axonotmesis
looks the same as in neurapraxic lesions (normal distal to site of lesion and smaller/absent CMAP proximal to the lesion)
At what point after trauma can you distinguish neurapraxic lesion from axonotmeis/neurotmesis?
After Wallerian degeneration has occured (about 9 days)
Changes in CMAP 10 days after a traumatic nerve injury with axonotmesis
CMAP with stimulation distal to the lesion will fall (Wallerian degeneration)
In traumatic axonotmesis/neurotmesis, which fails first, NMJ transmission or nerve excitability?
NMJ transmission
Inherent side to side variability in normals in CMAP amplitudes
Limitations of using CMAP amplitude to estimate number of surviving fibers after axonotmesis/neurotmesis
- inherent 30-50% side to side difference
- can only use early in injury before sprouting occurs
Percentage of axon loss estimations in mixed lesions in axonotmesis/neurotmesis are best done by...
comparing CMAP amplitude from distal stimulation with that obtained contralaterally
Conduction block estimates in in mixed lesions in axonotmesis/neurotmesis are best done by
comparing amplitudes or areas obtain proximal and distal to the lesion
F-waves are dependent on ___% of axons to elicit a resonse
Usefullness of F-waves in evaluation of traumatic nerve injuries
variable; may be useful in evaluation brachial plexus injuries where difficult to stimulate above and below the lesion
Which has a greater amplitude drop with distance of recording: CMAPs or SNAPs?
Factors that make SNAP amplitude decrease with distance
- temporal dispersion
- phase cancellation
Expected amplitude drop in SNAP over a 25cm distance
often 50-70%
Compare the timing of when you can see changes in sensory vs. motor nerve conduction in axonotmesis/neurotmesis
- 9 days for motor
- 11 days for sensory

* because NMJ transmission fails earlier than nerve conduction
Changes on needle EMG in neurapraxic lesions with complete conduction block
- No MUAPs on recruitment imemdiately after injury
- fibrillation potentials are controversial
Are NCSs very sensitive for picking up minimal axon loss?
Changes on needle EMG in neurapraxic lesions with incomplete conduction block
Reduced recruitment (decreased # of MUAPs firing more rapidly)
Are there morophology changes in MUAPs at any time after neurapraxic injuries?
No, there's no axon loss so there's no sprouting
Timing of onset of fibrillation potential and positive sharp after axonotmesis/neurotmesis injuries
* depends on length of nerve

- 10-14 days for short distal stump
- 21-30 days for longer distal stump (such as hand muscles in brachial plexopathy)
In general, what happens to fibillation potential size over time?
It decreases
Describe the specific changes that happen in fibrillation potentials over time with axonotmesis/neurotmesis injuries
- first few months: several hundred microvolts
- 1 year old: less than 100 microvolts
What happens to fibrillation potential frequency as a muscle is reinnervated? Is this generally clinically useful?
- decrease
- usually not useful (difficult to quantify, may be from muscle atrophy)
Does direct muscle injury cause fibrillation potentials?
How long can fibrillation potentials from direct muscle injury last
large range, but reported after biopsy to 11 months
What are the general changes in MUAP morphology that occur after axonal sprouting?
- amplitude: increase
- duration: prolonged
- polyphasic units: increased%
When does axonal spouting occur after axonotmesis/neurotmesis injuries?
- 4 days on pathological evaluation
- Seen on single fiber EMG studies at 3 weeks post-injury
After complete axonal loss, what are the first needle EMG findings of recovery?
MUAPs with:
- small amplitude
- polyphasic
- unstable
Which comes first with recovery after axonotmesis/neurotmesis injuries, EMG findings or clinical findings?
EMG findings usually occur before clinically evident voluntary movement
General approach to localizing traumatic nerve injuries
- detecting focal slowing or conduction block on NCSs
- pattern of denervation on EMG
Which type of traumatic nerve injuries can be well localized with NCS?
- able to stimulate above and below the lesion
- partial or complete neurapraxia or very acute axonal injuries
A patient has absent sensation but intact SNAPs after a traumatic nerve general, where is the injury?
proximal to the dorsal root ganglia
Trying to localize a traumatic nerve lesion based on nerve branching needs to also consider...
intraneural topography
Main electrodiagnostic tests used to differentiate root and plexus lesions in the brachial plexus
Paraspinal EMG and SNAPs
Describe the general order of mechanisms for recovery that contribute to increased functional muscle strength after a traumatic nerve injury
- resolution of conduction block
- distal axon sprouting
- muscle fiber hypertrophy
- axon regeneration
What limits the time that motor axonal regrowth can be expected to give functionally significant recovery?
18-24 months

After this the muscle has atrophied too much to respond even if nerve regrows
Remyelination after a neuropraxic lesion may take several _____
How fast can recovery occur after a Sunderland second degree traumatic nerve lesion?
- axons traverse segment in 8-15 days then regenerate along distal nerve segment at 1-5mm/day
Mixed traumatic nerve injuries often have a _____ phase recovery
2: initially fast phase, then slower
General prognosis of recovery in axonotmesis based on CMAP
* compare to contralateral side
<10% poor
10-30% good; not always complete
>30% excellent

(based on facial nerve; may even be more liberal in limbs)
How long should you wait to look for evidence of reinnervation in previously completely dennervatedmuscle near the site of a peripheral nerve traumatic lesion?
2-4 months
General steps involved in sensory recovery after traumatic peripheral nerve lesion
- resolution of conduction block
- redistribution of sensory function
- axonal regeneration
When is immediate surgical reconstruction indicated for traumatic peripheral nerve lesions?
sharp nerve laceration in who the nerve end are likely otherwise uninjured, complete injury
When is early (1 month)surgical reconstruction indicated for traumatic peripheral nerve lesions?
blunt trauma or avulsion with complete nerve disruption; sharp lesions that were not taken care of immediately

Usually only with complete lesions
In patients with axonotmesis with some spontaneous recovery, which is better: the natural recovery or recovery after surgical intervention
usually natural recovery course is better
When is delayed (3-6 months) surgical reconstruction indicated for traumatic peripheral nerve lesions?
when not clear if there is nerve continuity (traction injuries)
Nerve grafting 6 or more months after injury has a ____ surgical outcome
When is late (1+years) surgical reconstruction indicated for traumatic peripheral nerve lesions?
usually no functional recovery; may be done for pain control
How is the relative electrical magnititude mismatch between the motor neuron and muscle overcome?
By chemical transmission
How many times is the neuron's electrical signal amplified after transmission to the muscle?
Over 100-fold
What is the chemical transmitter at the neuromuscular junction?
Where is acetylcholine synthesized in nerve motor neurons?
in the nerve terminal
Acetylcholine is synthesized from _____ and ____ by the enzyme _____
synthesized from acetyl coenzyme-A and choline by the enzyme choline acetyltransferase
What are the 3 "compartments" of acetylcholine in the nerve terminal?
- reserve
- mobilization store
- synthesis
A quanta of acetylcholine likely contains how many molecules of acetylcholine?
Several thousand
The site on the motor neuron where Ach vesicles fuse is also called the _____ _____
active zone
Frequency of Ach quanta released by the motor neuron is dependent on
1. extracellular caldium concentration
2. temperature
Where are post-synaptic Ach receptors concentrated on muscle fibers?
At the crests of the post-synaptic folds across from the pre-synaptic active zones
Each Ach receptor requires the binding of how many molecules of Ach?
What is a MEPP?
- miniature endplate potential: postsynaptic nonpropagating depolarization
Acetylcholine is broken down by the enzyme _____ into ____ and ____
brokendown by the enzyme aceylcholinesterase into acetic acid and choline
The action of Ach on the post-synaptic membrane is normally terminated within _____
a few milliseconds
Depolarization of the nerve terminal causes an _____ of calcium
How many quanta are likely released after depolarization of a motor neuron?
around 100
Aproximate number of Ach receptor activated by Ach release from a depolarized motor neuron
100,000 Ach receptors
What is an EPP?
endplate potential; non-propagating depolarization of post-synaptic membrane (larger than MEPPs)
If an end plate potential exceeds the threshold for activation, what happens?
action potential propagated in both directions along the non-junctional muscle membrane
Generally speaking, what path does the action potential take to trigger muscle contraction?
along the membrane to transverse tubule system and voltage-sensitive calcium influx triggers mechanical cotnraction of the muscle fiber
What is the "safety factor" of neuromuscular transmission?
normally an excess of Ach is released and many more Ach receptors are activation beyond what would be needed for muscle contraction
Often often is myasthenia gravis associated with thymoma?
15% of patients
Reflexes in myasthenia gravis are
Sensation in myasthenia gravis is
Clinical presentation of myasthenia gravis is typically
Asymmetric weakness and fatiguability of extracular, bulbar, nuchal or limb muscles.
Antibodies in myasthenia gravis are directed at
Ach receptors; immune complexes are localized to the post-synaptic membrane
Antibodies to Ach receptors are detected in ____% of patients with myasthenia gravis
The number of Ach receptors on the post-synaptic membrane in myasthenia gravis is ____
Decreased number of Ach receptors in myasthenia gravis correlates with what electrodiagnostic finding?
MEPP amplitude in myasthenia gravis is about 1/5 of normal
Frequency of MEPPs is a function of what part of the synapse?
Frequency of MEPPs in myasthenia gravis is ____
Presynaptic Ach content and synaptic vesicles in myasthenia gravis are _____
What effects do anticholinesterases (cholinesterase inhibitors) have on EPPs?
- increased amplitude
- increased duration
- increased chance that EPP with reach threshold to cause an action potential
70% of cases of Lambert-Eaton Myasthenic syndrome are associated with _____
oat cell carcinoma of the lung
Typical muscle presentation of Lambert-Eaton Myasthenic syndrome
weakness/fatigability of proximal limb muscles with relative sparing of extraoccular and bulbar muscles
Reflexes in Lambert-Eaton Myasthenic syndrome
Lambert-Eaton Myasthenic syndrome is associated with what mucosal symptom?
dry mouth
On electron microscopy, what is disrupted in Lambert-Eaton Myasthenic syndrome?
The active zone is disrupted with decreased number of vesicles
MEPP amplitude in Lambert-Eaton Myasthenic syndrome is
Main problems in Lambert-Eaton Myasthenic syndrome
Presynaptic; fewer Ach quanta are released
EPPs in Lambert-Eaton Myasthenic syndrome are
MEPP frequency in Lambert-Eaton Myasthenic syndrome is
In Lambert-Eaton Myasthenic syndrome the decrease in EPP size is proportional to
decreased number of active zone particles
General definifion of congenital myasthenia
Collection of syndromes; muscle weakness and fatigue from birth, family history, no autoimmune myasthenia gravis in the mother and no Ach receptor antibodies in the child
In general, immunotherapy in congeital myasthenia is
not effective
Responses to anticholinesteraes in congenital myasthenia is
Familial infantile myasthenia usually presents with
severe respiratory and feeding problems
Proposed pathology for congential myasthenias
- deficient presynaptic Ach storage
- deficient presynaptic Ach mobilization
- deficient presynaptic Ach resynthesis
- reduced number of Ach receptors
- altered affinity of Ach ligands for receptors
Botulism is ____ mediated
Organism causing botulism
Clostridium botulinum
Typical presentation of infant botulism
- fail to suck/feed
- constipation
- weakness/hypotonia
Typical presentation of botulism in adults
descending paralysis, starting with the eyes
Extent of autonomic cholingergic involvement with botulism is determined by
the type of toxin
The onset of paralysis in botulism is faster in...
- nerves with high rate of firing
- increased temperature
Target of botulism toxin
irreversibly blocks Ach release; prevents vesicle fusion by some unknown mechanism
MEPP amplitude after botox A
normal; eventually decreased with huge doses
MEPP frequency after botox A
greatly reduced
Number of Ach quanta released after botox A is _____
greatly reduced
Ach synthesis in botulism is
Postsynaptic Ach sensitivity in botulism is
Recovery after botulism requires
- sprouting of new nerve terminals
- formation of new neuromuscular junctions
General definition of single fiber EMG
monitors action potentials of single muscle fibers extracellularly
Basic requirements of single fiber EMG (what do you need)?
- time base with resolution to microseconds
- stable trigger
- delay line
- method to record and count potentials
Duration of single fiber action potentials
1 millisecond
Peak-to-peak rise time of single fiber action potentials
100-200 microseconds
Amplitude of single fiber action potentials
1-5 microvolts
Muscle fiber density in neuromuscular disorders
usually normal
In normal muscle, pairs of potentials will be recorded about ____% of the time
On normal EMG what does recording a pair of potentials indicate
That you are recording 2 muscle fibers innervated by the same motor axon
What is the general definition of jitter
The variability in the interpotential interval between discharges
Normal jitter is between
10-60 microseconds
How is jitter usually expressed?
as the mean consecutive difference (MCD)
What produces most normal jitter?
fluctuations in the time the EPPs take to reach threshold for action potentials
In general, when is jitter increased?
- when the safety factor of neuromuscular transmission is lessened
- size of EPPs decreased
- rise time of EPPs decreased
At low rates of firing, increased jitter is a nonspecific measure of
neuromuscular dysfunction
What is blocking (related to jitter)
When one of the paired potentials fails to appear with the other
What is the underlying mechanism for blocking (related to jitter)
The EPP for the potential that did not show up, failed to reach threshold and therefore did not cause an action potential
Blocking is the single fiber EMG manifestation of clinical _____ and _____
fatigue and weakness
What is the most sensitive EMG finding of impaired neuromuscular transmission
increased jitter (although it's nonspecific)
In normal people, how does age influence jitter
Normal people over the age of 50 have increased jitter and blocking
What is abnormal jitter in the extensor digitorum muscle of the forearm?
- more than 1 in 20 pairs has MCD above 55 microseconds OR
- mean MCD of the 20 pairs is greater than 35 microseconds
Relation of jitter and firing rate in myasthenia gravis
increased jitter with increasing firing rate
Relation of jitter and firing rate in Lambert-Eaton myasthenic syndrome
decreased jitter with increasing firing rate
Relation of jitter and firing rate in botulism
decreased jitter with increasing firing rate
When is Ach supply depleted most prominantly during repetitive nerve stimulation in the normal nerve?
the first few stimuli when stimulated at 1-4 Hz (after that mobilization stores have replenish the supply)
What is the effect of calcium on repetitive stimuli less than 200milliseconds apart?
Calcium from previous impulse still around to help facilitate transmission
Why does facilitation through calcium of neurotransmission decreased at 50Hz and 200Hz?
50: impulses begin to overlap each other
200: exceeds refractory period of muscle and nerve
Optimal stimulation rate for calcium facilitation in Lambert-Eaton myasthenic syndrome and botulism
40-50 Hz
Why is a drop in MUAP amplitude on routine EMG not a good indicator of NMJ disease?
Because the change is more likely to be from needle movement than blocking
Why can amplitude increase again after 5 or so repetitive stimuli during EMG study in myasthenia gravis at rest?
Presumably Ach mobilization has caught up with the depletion
Voluntary exercise typically creates a stimulation rate of ___ Hz
20-50 Hz
Tetanic external stimulus is delivered at ___Hz
50 Hz
What is postactivation potentiation in myasthenia gravis?
The size and areas of evoke response may be larger and the decrement less immediately after exercise secondary to calcium facilitation
What is psedofacilitation is comparison to postactivation potentiation?
Increased amplitude after exercise because of greater synchronization; area of the response remains the same.
What is post-activation exhaustion in myasthenia gravis?
A few minutes after exercise the size of the response is smaller and the decrement with repeat stimulation greater
Post-activation exhaustion in myasthenia gravis is attributed to
receptor desensitization
Often the only electrodiagnostic finding in mild myasthenia gravis may be
post activation exhaustion (measure every minute after exercise for 5 minutes)
Is repetitive nerve stimulation a sensitive test for myasthenia gravis?

For example ~30% of patients with definitive MG may have normal repetitive nerve stimulation findings
Is repetitive nerve stimulation a sensitive test for Lambert-Eaton myasthenic syndrome?
CMAP at rest in Lambert-Eaton myasthenic syndrome is usually ____% of normal
2 electrodiagnostic hallmarks of Lambert-Eaton myasthenic syndrome
- postactivation potentiation
- low amplitude initial response
What happens to the initial/early response in Lambert-Eaton myasthenic syndrome with slow stimulation?
Further Ach depletion occurs and there is a decremental response
If postactivation potentiation is greater than 200%, what 4 conditions should you think of?
- Lambert-Eaton myasthenic syndrome
- botulism
- hypermagnesemia
- hypocalcemia
In Lambert-Eaton myasthenic syndrome, what muscle typically display the typical electrodiagnostic findings?
ALL limb muscles
Do decremental responses with slow rates of stimulation typically occur in botulism?
Electrodiagnostic findings typical of moderate botulism
- postactivation potentiation
- incremental responses to high rates of stimulation

* indicate that neurotransmitter release can be increased with repeated stimulation
Electrodiagnostic findings typical of severe botulism
- small initial response
- no post-activation potentiation
- no incremental response
In botulism, which muscles typically show electrodiagnostic abnormalities?
Why is repetitive nerve stimulation often a useful test in botulism?
Electrodiagnostic changes are usually evident several days before toxin can be identified in the lab
Regular EMG findings typical for infantile botulism
Within a few day, see short-duration low amplitude polyphasic motor units with spontaneous activity
What are the guidelines for holding medications prior to testing for NMJ disorders
hold anticholinesterase medications for 24 hours prior to test if it does not compromise the patient's swallow or respiratory status
Why does cooling improve transmission in NMJ disorders?
- acetylcholinesterase activity is less when colder
Does limb temperature matter in repetitive nerve stimulation?
Yes, NMJ transmission may appear falsely normal if the patient is cold
In myasthenia gravis, which muscles are more likely to show abnormalities on repetitive nerve stimulation: distal or proximal?
proximal (think of proximal muscles as being warmer)
What kind of stimulation do you use in repetitive nerve stimulation for NMJ disorders?
Supramaximal at 25% greater than the stimulus where no change in amplitude is observed
In general, what stimulus do you deliver during repetitive nerve stimulation?
At least 4 supramaximal stimuli at a rate of 2-3 Hz
In general, how long do you wait between trains of stimuli in repetitive nerve stimulation?
15 seconds
What % change for decrement in repetitive nerve stimulation is considered abnormal
5% likely
10% certainly
List the levels and numbers for spinal roots
C 8
T 12
L 5
S 5
Cox 1
Where are the cell bodies of the nerves that form the ventral roots of the spinal nerve?
In the anterior and lateral gray columns
Where are the cell bodies of the dorsal roots of the spinal nerve?
In the dorsal root ganglia
Where does the dorsal root ganglia lie anatomically?
In the ostium of the bony intervertebral foramina
What do the posterior primary rami of the spinal nerves supply?
segmental paraspinal muscles and skin
What are the rules for where the cervical nerve roots exit compared to vertebral level?
C1-C7 exit superiorly, C8 exits below C7 vertebral body
What are the rules for where the thoracic and lumbar nerve roots exit compared to vertebral level?
exit at below the vertebral level of the same number
The sensory fibers composing the cauda equina are __-ganglionic
Radiculopathy in patients under 40-50 years old is usually from
intervertebral disk protrusions or ruptures
Radiculopathy in patients over 50 years old is usually from
osseoligamentous hypertrophy
What are the most common motor vs. sensory presentations of radiculopathy
sensory > mixed > motor
How does conduction block in radiulopathy usually manifest clinically?
short-lived but profound weakness
What is the presumed mechanism of slowing in radiculopathy when deep tendon reflexes are lost but there is no weakness or sensory loss?
desynchronized or differential slowing
What is more characteristic of radiculopathy: subtotal or total root involvement?
subtotal root involvement
Single motor and sensory NCS in radiculopathy are usually _____
When there is nerve damage proximal to the DRG, nerve degeneration proceeds in which direction?
Why are SNAPs normal in radiculopathies?
because the injury is proximal to the DRG
What is the only abnormality on NCS that may occur with radiculopathy
decreased amplitude of the CMAP if there is axon degeneration
Why are CMAPs on NCS usually normal in single level radiculopathy?
- incomplete nerve root involvement
- muscles innervated by more than one root
Abnormal H-wave latency criteria that reflect S1 radiculopathy
1.0-1.8 ms side to side difference, or outside of normal predicted by nomogram
Abnormal H-wave amplitude criteria that reflect S1 radiculopathy
side-to-side reduction of amplitude of 50% or unable to elicit response
5 limitations of using H-waves in the diagnosis of radiculopathy
- only S1 used
- may be normal with radic
- abnromal H-wave does not equal radic
- once H-waves lost, often remain so
- often unelictable bilaterally in polyneuropathy
H-waves in normal people over the age of 60 are often
unelictable bilaterally
F-waves are generally ___% of the size of the direct muscle response
less than 5%
For F-waves, minimal latency is assumed to represent
conduction time along one of the largest diameter motor fibers in the stimulated nerve
Are SEPs helpful in the diagnosis of radiculopathy?
Usually not, relatively insensitive
In the evaluation of radiculopathy, the needle electrode examination (NEE) is primarily evaluating what?
motor root fibers for the occurance of axon loss
How many muscles are required in a "radiculopathy screen."
5-7 including paraspinals
Ideally, what are consititues a positive needle screen for radiculopathy?
Findings in 2 or more muscles that receive innervation from the same root
- ideally via different peripheral nerves
- neighboring myotomes normal
What is the deepest paraspinal muscle?
The multifidus
Which paraspinal muscle is the only one considered to have monosegmental innervation?
The multifidus
In general, paraspinal muscle sampling in radiculopathy screen should be done at and ___ the level of the lesion
Effect of age on spontaneous fibrillation potentials seen in paraspinals of normals
increase with age, especially over 40
% of normal people with fibrillation potentials in paraspinals
15-50%, increases with age
List conditions other than radiculopathy that may cause fibrillation potentials in the paraspinal muscles
- motor neuron disease
- muscle trauma (LP, steroid injections, surgery)
- tumors
- toxic/inflammatory myopathies
- diabetes
The inside of a muscle cell is relatively ______ in charge compared to the outside
Why can you detect voltage in a depolarizing cell?
No longer a perfect balance of +/- charges in the region of depolarization and thus can detect a voltage difference
Key ions for detecting voltage change in EMG?
Na+ and K+
Voltage = ()x()
Voltage = Current x Impedence
In EMG what is the zero reference?
the ground
The magnitude and polarity of a recorded EMG potential depend on what 4 key factors?
- charge density near the membrane
- distance from depolarization
- properties of the medium
- location of measurement
What is Fourier analysis?
It's a frequency analysis that characterizes a waveform by its frequency components
CMAPs are ____ duration
SNAPs are ____ duration
Give 3 examples for waveforms that have fast changing components (high frequency)
- Fibrilations
- Polyphasic motor units
- single fiber EMG
Give 4 examples for waveforms that have slow changing components (low frequency)
- the positive part of positive sharp waves
- SEPs
Give 3 common general sources for electrical noise on EMG
- radio
- 60 Hz
- electrical equipment
The signal for EMG is typically amplified ______ times
What is the voltage requirement for a signal to be respresented reasonably in analog?
1-10 volts
Define gain
electrical amplification of the signal
Define sensitivity
display resolution
Why do we use a differential or instrumentation amplifier?
to reject environmental noise
Define common mode signal
signal that appears with equal amplitude at both the recording and reference electrodes
What is the common mode rejection ratio?
for the amplifier: the gain of the physiologic potential/the gain of the noise signal
What common mode rejection ratio do you want in an EMG amplifier?
at least 90 dB
What is the main function of filters in EMG?
noise attenuation
Why is the low frequency filter in single fiber EMG increased to 500 Hz?
To filter out more distant motor units
What does a filter setting really mean?
The point where 1/2 of the energy is removed
Do filters cause phase shift?
Where is phase shift from filters the most pronounced?
near the filter limit
What are the typical filter settings for motor NCS?
2-10,000 Hz
What are the typical filter settings for sensory NCS?
5-2,000 Hz
What are the typical filter settings for EMG?
10-10,000 Hz
What are the typical filter settings for quantitative EMG?
2-10,000 Hz
What are the typical filter settings for SSEP?
5-2,000 Hz
Lowering the high frequency filter will have what effect on the CMAP?
- decrease amplitude
- reduce polyphasia
Lowering the high frequency filter will have what effect on SNAP?
- decrease amplitude
- prolong latency
Lowering the high frequency filter will have what effect on the triggering of the instrument to record a potential?
- increase the magnitude of change needed to trigger the recording
What is the effect of increasing the change needed to trigger an EMG recording?
Increased onset latency
Why is the filter range for SNAPs smaller than that for CMAPs?
More important to reduce noise
What percentage of SNAP amplitude is lost with typical standard filters?
Soft tissue acts as what type of filter?
high frequency
Increasing the low frequency filter will have what effect on the CMAP?
- decreased amplitude
- poor tracking of return to baseline so wave form gets distorted
- shorter peak latency (returns to baseline sooner)
Lowering the high frequency filter will have what effect on the SNAP?
same effects as on CMAP but less pronounced:
- amplitude loss
- wave form distortion
- shorter peak latency
Lowering the high frequency filter will have what effect on the MUAPs?
- prolonged duration from trailing negative hump
- decreased amplitude
- decreased duration
Do most waveforms have significant 60 Hz components?
When digitizing a signal, how often should you sample?
Twice the rate of your highest filter (so if filter is 10K then need to sample at least 20K).
You need good electrodes for EMGs so that...
they create stable polarization potentials on the skin that are reliable for analysis
When the recording electrode is placed right over the motor point the waveform tends to have these characteristics:
- clean take-off
- biphasic morphology
- initially negative
SNAPs with the A&R electrodes less than 4cm apart will ____
have decreased amplitude
Why do SNAP A&R electrodes need to be at least 4cm apart?
4cm is the length of nerve that is in a depolarized state assuming a 50m/s conduction velocity and 0.8ms depolarization duration.
In needle EMG with a monopolar electrode, the impedence of the reference is usually ______ fold lower
10 fold
Why does needle EMG with a monopolar electrode have more 60 Hz interferrence?
The 10 fold difference in impedence at the recording and reference electrodes makes common mode rejection difficult
Skin reference for monopolar electrodes should be placed...
over a local bony or tendon site; if lots of interference then place closer to the needle
Typical tip area of a monopolar electrode
Typical tip area of a concentric electrode
The recording area of a concentric electrode is determined by
- wire diameter
- angle of the bevel
What is the diameter of a typical muscle fiber?
60 micrometers
Compared to monopolar electrodes, concentric electrodes record _____ amplitudes.
smaller (about 1/2 as large)
Compared to monopolar electrodes, concentric electrodes record _____ phasicity
Compared to monopolar electrodes, concentric electrodes record _____ duration
Why is the amplitude recorded by concentric electrodes smaller than monopolar?
recording surface and proximity of reference to active
Why is the phasicity recorded by monopolar electrodes more than concentric?
larger recording distance = less synchrony
The EMG machine analyzes signal by subtracting...
active - reference
The duration of a waveform depends most on what frequency components?
Why do we use impedence in EMGs instead of resistence?
Becuase the current fluctuates (use resistance with stable current like batteries).