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Emg Flashcards

1
Q

Describe the make up of the nerve connective tissue:

A

Axon –> myelin sheath –> endoneurium (surrounds individual axon/myelin) –> perineurium ( strong protective layer surrounding bundles or fascicles of myelinated and unmyelinated nerve fibers) –> epineurium ( loose connective tissue surrounding entire nerve, protects from compression)

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2
Q

What is the function of the perineurium in nerve connective tissue?

A

Strong protective connective tissue surrounding bundles or fascicles of myelinated and unmyelinated nerve fibers. Helps to strengthen the nerves and acts as a diffusion barrier. Individual axons may cross from one bundle to another along the course of the nerve.

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3
Q

Name the five components of the motor unit

A 
Anterior horn cell (motor nerve cell body) 
Motor nerve axons 
Peripheral nerve 
Neuromuscular junction 
Muscle fibers
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4
Q

Name the three types of motor neurons

A

Alpha - extrafusal (skeletal muscles)
Gamma - intrafusal (muscle spindle)
Beta - intrafusal and extrafusal

Emg can only study alpha motor neurons

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5
Q

The order of recruitment of muscle fibers is related to:

A

Size, starting with the smaller motor units. (Known as henneman size principle) allows for smooth increase of contractile force

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6
Q

What is the Henneman Size Principle?

A

A smaller alpha motor neuron has a low threshold of excitation, causing it to be recruited first during voluntary contraction.

A larger alpha motor neuron has a higher threshold of excitation and is recruited when more motor units are needed to generate a greater contractile force.

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7
Q

There are two types of muscle fibers, Type I and II. Describe four Intervation characteristics for each

A 
Type I:
  Smaller cell body 
  Thinner diameter axon 
  Lower Intervation ratio
  Slow twitch muscle fibers 
Type II: 
  Larger cell body 
  Thicker diameter
  Higher Intervation ratio 
  Fast twitch muscle fibers
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8
Q

Lloyd and Hunt classification of nerve fibers

A

Ia, Ib, II, III, IV fibers

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9
Q

Of the Loyd and Hunt (sensory) classification describe type Ia and Ib fibers

A 
Ia   (A-alpha fibers) 
10-20um diameter  (largest) 
50-120m/sec (fastest) 
Function: 
- motor: alpha motor neuron
- sensory: muscle spindle (gamma) 
Ib (A-alpha fibers) 
10-20um
50-120m/sec
Function: 
- sensory: Golgi tendon organ, touch, pressure
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10
Q

Of the Loyd and Hunt (sensory) classification, describe the II, III, IV fibers

A

II
4-12um (A-beta)
25-70m/sec
Function:
- motor: intrafusal and extrafusal muscle fibers
- sensory: muscle spindle, touch, pressure

III
2-8um (a-gamma) and 1-5um (a-delta)
10-50m/sec and 3-30m/sec
Function 
- motor: gamma motor neurons, muscle spindle
- sensory: touch, pain, temp 
IV
1-3um (B-fibers) and <2m/sec
Function
- motor: postganglionic autonomic fibers, pregabglionic autonomic fibers 
- sensory: pain, temperature
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11
Q

Function of Ia fibers (A- alpha fibers)

A

Motor - alpha motor neurons

Sensory - muscle spindle

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12
Q

Function of Ib (A-alpha fibers)

A

Sensory: Golgi tendon organ, touch, pressure

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13
Q

Other muscle fiber classification besides Lloyd and Hunt (sensory)

A

Erlanger and Gasser (sensory and motor)

A-alpha, A-beta, A-gamma, A-delta, B-fibers, C-fibers

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14
Q

Resting membrane potential:

A

Voltage of axons cell membrane at rest.

-70 to -90mV

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15
Q

What are leak channels

A

Openings in the cell membrane that allow sodium and potassium to move passively in and out of the cell membrane.

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16
Q

What is the Intervation Ratio?

Varies depending on:

Explain high and low ratio.

The higher the IR, the greater the:

A

The amount of muscle fibers belonging to an axon

Varies depending on function.

Muscles of gross movement have larger amount of their fibers innervated by one axon (high ratio) - ex: leg muscle 600:1

Muscles of fine movement have a smaller amount of their fibers innervated by one axon (low ratio) - ex: eye muscle 1:1

The higher the IR, the greater the force generated by a motor unit

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17
Q

Sodium channels remain open for how long?

Change in decrease temp?

A

Remain open for approximately 25 microseconds.

A decrease in temp affects the protein configuration and causes a delay in opening and closing of the gates.

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18
Q

Waveform appearance due to decrease in temperature

Latency:
Amplitude: 
Duration: 
Conduction: 
Velocity:
A

Prolonged
Increased
Increased
Decreased

Generalized cooling is worse in these areas than local cooling except the amplitude is not different from normal testing temp (33 or 31) and negative spike duration is slightly less than focal cooling.

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19
Q

What is saltatory conduction?

A

As sodium goes into the cell for depolarization, it moves away from the membrane and spreads the current down a path of least resistance along the length of the axon. The affinity to flow back out through the membrane is low due to the myelin sheath covering. Thus, the potential “jumps” to the next group of sodium channels,located between the myelin, to areas called the nodes of ranvier. This process of propagating a current from one node to another is known as saltatory conduction.

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20
Q

Explain overshoot phenomenon as it pertains to potassium voltage hated channels

A

After a slight delay, these channels open from a depolarization. This allows K to move out of the cell to establish a charge equilibrium. A delay exists in channel closure which results in a membrane with a hyper polarized state called an overshoot phenomenon. This process of potassium conductance eventually returns the waveform to its baseline due to the K leak channels restoring the RMP

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21
Q

NMJ has what three components?

A

Presynaptic region - ACH storage and migration
Synaptic cleft - contains acetylcholinesterase
Post synaptic region - lined with ACH receptors

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22
Q

The Presynaptic region of the NMJ contains ACH in what three storage compartments?

ACH is stored in packets called:
These hold _____ molecules

A

Main store - 300,000 quanta
Mobilized store - 10,000 quanta
Immediate store - 1,000 quanta

Quanta - 5,000 - 10,000 molecules

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23
Q

ACH migrates in the Presynaptic region from main and mobilization storage to replenish immediate storage compartments which takes approximately _____

A

4-5 seconds

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24
Q

Synaptic cleft of the NMJ contains what enzyme? Reaction?

A

Acetylcholinesterase convert acetylcholine into acetate and choline as it crosses the cleft.

Cleft is 200-500 angstroms wide

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25
Q

Describe sodium-potassium ATP dependent pumps

A

Negative potential is maintained inside the cell by actively exporting 3 sodium ions and importing 2 potassium ions through the pump. This keeps each ion against a concentration gradient with a deficit of positive ions inside the cell. The resting membrane potential of the nerve would otherwise dissipate from the ions diffusing through the ion leak channels

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26
Q

Neuromuscular junction physiology:
1 During resting state, a spontaneous release of quanta (5,000-10,000 molecules of ACH) occurs every ____.

  1. During an excited state, a nerve depolarization opens ____ channels which causes flooding into the nerve channels lasting ____.
  2. During excited state MEPPs accumulate to form _______
A
  1. every 5 seconds - results in one miniature endplate potential (MEPP)
  2. Voltage-gated calcium channels; 200msec – leads to release of multiple quanta into the synaptic cleft, which increases the amount of MEPPS.
  3. an endplate potential (EPP) which generates a motor unit action potential (MUAP)
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27
Q

What is the Quantal content?

What is Quantal Response?

A
  1. This is the number of ach quanta released with each nerve depolarization .
  2. This is the ability of the ACh receptors to respond to the ACh molecules that are released.

Has to do with the “safety factor” - which is the initial excess amplitude of EPP which allows time for acetylcholine to move from main to mobilizing storage compartments to replenish the immediate storage compartment. This avoids the drop of the EPPs amplitude below the threshold needed to cause an action potential

The safety factor depends on these two parameters

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28
Q

A cylindrical, multinucleated cell containing contractile elevments composed of actin and myosin:

A

skeletal muscle fiber

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29
Q

A ____ is teh basic unit of a muscles myofirbril. It runs from ____ line to ____line.

A

Sarcomere; z line to z line

its size changes during contraction.

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30
Q

Muscle fiber characeteristics depend on _____

If a muscle fiber becomes denervated, it will: ______

A

motor unit by which it is innervated.

Take on the characteristics of the alpha motor neuron that reinnervates it.

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31
Q

Type I Muscle fibers

  1. Alpha motor neuron:
  2. Color:
  3. Recruitment:
  4. Fatigue:
  5. Effort:
  6. Firing frequency:
  7. Movements:
  8. Innervation ratio:
  9. Amplitude/Duration:
  10. O2 capacity:
A

Type I (SO) Slow Twitch Oxidative

  1. Small
  2. Dark
  3. Early
  4. Highly resistant
  5. Mild (4-8hz)
  6. Slow, prolonged
  7. Fine, precise
  8. small
  9. small
  10. aeorbic
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32
Q

Type IIA muscle fibers

  1. Alpha motor neuron:
  2. Color:
  3. Recruitment:
  4. Fatigue:
  5. Effort:
  6. Firing frequency:
  7. Movements:
  8. Innervation ratio:
  9. Amplitude/Duration:
  10. O2 capacity:
A

Fast twitch oxidative-glycolytic

  1. Large
  2. Dark
  3. Late
  4. Resistant
  5. Intermediate (20-30hz)
  6. Fast, unsustained
  7. Gross
  8. Large
  9. Large
  10. Anaerobic
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33
Q

Type IIB muscle fibers:

  1. Alpha motor neuron:
  2. Color:
  3. Recruitment:
  4. Fatigue:
  5. Effort:
  6. Firing frequency:
  7. Movements:
  8. Innervation ratio:
  9. Amplitude/Duration:
  10. O2 capacity:
A

Fast Twitch Glycolytic

  1. Large
  2. Pale
  3. Late
  4. Sensitive
  5. High (20-30hz)
  6. Fast, Unsustained
  7. Gross
  8. Large
  9. Large
  10. Anaerobic
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34
Q

The stimulus of muscle fiber depolarization for muscle contraction spreads in both directions on the fiber at _____.

It penetrates deeper into the muscle via the _____.

This causes Ca to be released from the ______.

It binds to the _____ complex and exposes actin’s active sites.

_____ bind with these active sites.

______ and ____ slide over each other to shorten the muscle.

A

3-5 meters per second

T-tubule system

sarcoplasmic reticulum

troponin-tropomyosin complex

myosin heads, powered by ATP, bind with active sites.

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35
Q

relaxation after muscle contraction is powered by ____.

____ is actively pumped back into the cell.

This allows ______ to block actin’s active sites

A

ATP

Ca

tropomyosin

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36
Q

Absence of ATP in muscle fiber relaxation leads to _____. Due to:

A

Rigor Mortis; due to actin and myosin filaments remaining permanently joined.

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37
Q

______ increases the membrane capacitance due to the loss of myelin insulation, thus hindering salutatory conduction.

A

demyelination

Na leaks out due to no myelin covering on the nerve so no longer has need to jump from node to node (of ranvier)

This translates to slower nerve conduction.

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38
Q

With demyelination, describe acute phase and chronic phase

A

acute - trophic factors of the nerve are maintained, and myelin regeneration is possible due to schwann cell proliferation. Acutely, conduction block occurs

Over time, remyelination can occur. This can become a cycle.

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39
Q

Define conduction block

A

failure of an action potential to propagate past an area of demyelination along axons that are otherwise structurally intact.

presents as 50% drop in CMAP amplitude between proximal and distal stimulation sites across the area of injury.

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40
Q

Etiology of demyelination?

A

compression causing a transient ischemic episode, edema, or myelin invaginations with paranodal intussusceptions

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41
Q

Diseases causing degradation of myelin lead to ____.

A

peripheral neuropathies

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42
Q 
Electrodiagnostic findings of demyelination: 
NCS
Latency: 
Conduction velocity: 
Temporal dispersion: 
Amplitude
A

Latency: prolonged
Conduction velocity: Decreased
Temporal dispersion: Increased
Amplitude: decreased across site of injury

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43
Q 
Electrodiagnostic findings of demyelination: 
EMG: 
Insertional activity: 
Resting activity: 
Recruitment: 
MUAP:
A

Insertional activity: Normal
Resting activity: Normal +/- myokymia
Recruitment: +/- decreased
MUAP: normal

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44
Q

Recovery of demyelination is ____

A

self limited. pathology can reverse with cessation of the insulting event. Transient ischemia can be immediately reversed but edema can take several weeks.

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45
Q

New myelin in remyelination is ____ and ____ than compared to original. ____ improves but is usually slower than normal

A

thinner; shorter internodal distances. Conduction velocity.

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46
Q

two forms of axonal injury presentation. define both

A
  1. Axonal degeneration: a nerve injury that begins in a “dying back” fashion and affects the nerve in a length dependent manner. Starts distally and ascends proximally
  2. Wallerian Degeneration: at the site of the nerve lesion, the axon degenerates distally. The nerve segment proximal to the injury site is essentially intact with some minor dying back at the lesion site 1-2cm.
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47
Q

In Wallerian degeneration:

  1. In distal motor axons, degeneration is generally complete in:
  2. For distal sensory axons, degeneration is generally complete in:
A
  1. 7 days (motor/distal)

2. 11 days (sensory/distal)

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48
Q

Axonal injuries can occur from: (4) etiologies

A
  1. focal crush
  2. stretch
  3. transection
    4 peripheral neuropathies
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49
Q

Name the stages of axonal injury:

A

I Normal nerve cell
II post injury - nissl substance degenerates
III swollen cell body with eccentric nucleus
IVa cell deth
IVb cell recovery

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50
Q 
Electrodiagnostic findings of axonal injury
NCS
Latency: 
Amplitude
temporal dispersion
conduction velocity
A

latency: Normal
amplitude: Decreased
temporal dispersion Normal
conduction velocity: Mildly decreased

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51
Q 
Electrodiagnostic findings of axonal injury
EMG
Insertional activity
resting activity
recruitment
MUAP:
A

Insertional Activity: Abnormal
Resting activity: Abnormal
Recruitment: Decreased
MUAP: Abnormal

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52
Q

______ is a process in which a neurite sprouts off the axon of an intact motor unit and innervates denervated muscle fibers of an injured motor unit

A

axonal sprouting

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53
Q

Describe axonal sprouts in three ways

A

smaller terminal branches
thinner myelin
weaker neuromuscular junctions

Increased fiber type grouping occurs as muscle fibers become part of the new motor unit and take on its characteristics, increasing the size of its territory. This remodeling results in motor units with poor firing synchronicity, secondary to the immature terminal sprouts. This results in polyphasic waveforms with increased amplitudes.

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54
Q

What does axonal sprouting look like on EMG?

A

Polyphasic waveforms with increased amplitudes: Increased fiber type grouping occurs as muscle fibers become part of the new motor unit and take on its characteristics, increasing the size of its territory. This remodeling results in motor units with poor firing synchronicity, secondary to the immature terminal sprouts. This results in polyphasic waveforms with increased amplitudes.

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55
Q

Define axonal regrowth

A

process of repair in which the axon will regrow down its original pathway toward its muscle fibers.

1mm per day
1 inch per month (35mm per month)
if the supporting connective tissue remains intact.

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56
Q

Describe quality of axonal regrowth

A

decreased diameter
thinner myelin
shorter intermodal distance

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57
Q

What does axonal regrowth look like on EMG

A

with reinnervation, low amplitude, long duration, polyphasic potentials known as nascent potentials are formed.

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58
Q

What happens if connective tissue is not strong enough to support axonal regrowth?

A

A neuroma can form with failure to reach the final end organ. Concomitantly the shorter the distance from the injury to end organ, the higher the likelihood for a better prognosis.

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59
Q

In axonal injury recovery:

Collateral sprouting vs axonal regrowth - who prevails?

A

If an axon re-grows to innervate its original muscle fibers, but collateral sprouting to these fibers has occurred, the nerves possessing the largest axon, thickets myelin, and strongest NMJ will prevail and keep the muscle fibers.

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60
Q

Motor unit remodeling: (describe what occurs and MUAP mV)

  1. Normal TI and TII fibers - MUAP mV:
  2. 2-3 wks post degen:
  3. 1-2 months
  4. 2-6 months
  5. 6months - 2 yrs
A
  1. 600mV
  2. TII fibers degen. TI still yields 600mV action potential
  3. TII atrophies, TI collateral sprouting begins.
    TI unit territory subsequently collapses due to TII atrophy. causes increase in MUAP: 1200mV
  4. as connections mature, MUAP increases 7000mV and you have polyphasic waves. By 6 months, all muscle fibers belonging to TI motor units are of the same fiber type. (TII are now TI)
  5. as maturity occurs, MUAP may decrease its amplitude and phases due to collaterals conducting potentials more rapidly. 6000mV
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61
Q

Name the 2 types of nerve injury classification systems

A
  1. Seddon Classification

2. Sunderland Classification

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62
Q

Name the three types of the Seddon classification and their etiology

A
  1. Neuropraxia - Nerve compression injury
  2. Axonotmesis - Nerve crush injury
  3. Neurotmesis - nerve transection injury
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63
Q 
Seddon classficiation of N injury
1. Neuropraxia: 
Etiology: 
Description of injury: 
NCS
EMG:
A

Etiology: nerve compression injury
Description: Axon intact, Local myelin injury, conduction block
NCS: signal is normal distal to lesion and abnormal across it.
EMG: normal/decreased recruitment

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64
Q 
Seddon Classification of N injury
2. Axonotmesis
Etiology
Description of injury
NCS:
EMG:
A

Etiology Nerve crush injury
Description: Axonal interruption, connective tissue/schwann cell intact, conduction failure
NCS: conduction resembles neuropraxia for 4-5 days, until wallerian degeneration occurs
EMG: abnormal

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65
Q 
Seddon Classification of N injury
3. Neurotmesis 
Etiology: 
Description of injury
NCS: 
EMG:
A

Etiology: nerve transection injury
Description: Axonal interruption, Connective tissue disruption, Conduction failure
NCS: Conduction initially resembles axonotmesis, but does not resemble recovery
EMG: Abnormal activity

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66
Q

Name the 5 types of the Sunderland classification and their etiologies

A 
Type I Conduction block - neuropraxia
Type II Axonal injury - axonotmesis
Type III Type 2 + endoneurium injury
Type IV Type 3 + perineurium injury
Type V Type 4 + epineurium injury (neurotmesis)
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67
Q

Electronic circuitry passes through the wire based on Ohms law: describe

A

current = voltage/resistance

Resistance (impedance) caused by skin lotions, oils, gels, etc.

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68
Q

In a sensory N study, the recording electrode is placed _____.
In a motor N study, the recording electrode is placed ____.

A

for SNAP - placed directly over the nerve

for CMAP - placed over the motor endplate of a muscle that is innervated by that nerve.

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69
Q

What is a CMAP?

A

compound muscle action potential - is the summation of electrical activity generated by muscle fibers; it is an indirect representation of electrical activity generated by a motor nerve

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70
Q

_____ is a 22 to 30 gauge Teflon-coated needle with an exposed tip of 0.15-0.2mm^2.

A

Monopolar needle electrode

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71
Q

Monopolar needle electrode
Advantages (5)
Disadvantages (4)

A

Advantages:

  1. inexpensive
  2. conical tip - Omni-directional recording
  3. Less painful (Teflon decreases friction)
  4. Larger recording area (2 x concentric)
  5. Records more positive sharp waves and more abnormal activity in general

Disadvantages:

  1. requires a separate needle or surface reference
  2. nonstandardized tip area
  3. Teflon fraying
  4. may have more interference if the reference is not near the recording electrode.
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72
Q

____ is a 24 to 26 gauge needle (reference) with a bare inner wire (active)

A

Standard concentric (Coaxial) needle electrode

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73
Q

Advantages (5) and disadvantages (4) of standard concentric (coaxial) needle electrode

A

Advantages:

  1. standardized exposed area
  2. fixed location from reference
  3. no separate reference
  4. used for quantitative EMG

Disadvantages:

  1. Beveled tip: unidirectional recording
  2. smaller recording area
  3. motor unit action potentials have smaller amplitudes
  4. more painful
74
Q

_____ is a needle with the active and reference wires within its lumen

A

bipolar concentric needle electrode

75
Q

Advantages (2) and disadvantages (2) of bipolar concentric needle electrode

A

Advantages:

  1. best for isolating MUAP
  2. less artifact

Disadvantages

  1. expensive
  2. more painful
76
Q

_____ is a needle (reference) consisting of an exposed 25um diameter wire (active)

A

single fiber needle electrode

77
Q

Advantages (6) and disadvantages (2) of single fiber needle electrode

A

advantages

  1. looks at individual muscle fibers
  2. used to assess fiber type density
  3. used to assess jitter
  4. used to assess fiber blocking
  5. helpful in NMJ disorders
  6. Helpful in motor neuron disorders

disadvantages

  1. not used for traditional emg
  2. expensive.
78
Q

____ is a theoretical local block that occurs when reversing the stimulators cathode and anode. This hyperpolarizes the nerve, thus inhibiting the production of an action potential

A

anodal block

79
Q

______ occurs when the stimulus current spreads through tissue surrounding the nerve.

A

volume conduction. Occurs if a stimulus is set too high.

80
Q

In volume conduction due to too high of a stimulus, skin, extracellular fluid, muscles, and other nerves may be stimulated which can lead to: (3)

A
  1. decreased conduction times and shortened latencies
  2. altered waveforms
  3. amplitudes remain unchanged
81
Q

Usually stimulus duration is set at ______ and may be increased incrementally to ensure supramaximal stimulation. If a monopolar needle is used for stimulation, start at _____.

A
  1. 1 milliseconds
  2. 5 milliseconds

longer stimulus duration will cause more pain

82
Q

______ refers to selectively amplifying different signals and rejecting common ones. It is usually expressed as decibels (dB) and should be 90dB or greater.

A

common mode rejection ratio (CMRR). the larger this is, the more efficient the amplifier

83
Q

Filter settings: (in Hz)
Sensory NCS:
Motor NCS:
EMG:

A

Sensory: 20 Hz - 10kHz
Motor: 2hz - 10kHz
EMG: 20Hz - 10kHzh

84
Q

Effects of elevating the low frequency filter (4)

A

high pass

  1. reduces the peak latency
  2. reduces the amplitude
  3. changes potentials from bi- to triphasic
  4. does not change onset latency
85
Q

effects of reducing the high frequency filter (4)

A

(low pass)

  1. prolongs the peak latency
  2. reduces amplitudes
  3. creates a longer negative spike
  4. prolongs the onset latency
86
Q

Screen:
EMG/NCS:
horizontal axis represents: ___
Vertical axis represents: ____

A

sweep speed

sensitivity

87
Q

______ pertains to the time allocated for each x-axis division and is measured in milliseconds

A

sweep speed

88
Q

_____ pertains to the height allocated for each y-axis division and is measured in millivolts (mV) or microvolts (uV).

A

sensitivity/gain

89
Q

____ is a ratio of measurement of output to input and does not have a unit value such as mV or uV. Sometimes used interchangeably with sensitivity

A

gain

90
Q

Settings for sweep speed:
sensory:
motor:
EMG:

A

5ms
2ms
10ms

91
Q

settings for sensitivity
sensory:
motor:
EMG:

A

10uV
5mV
100uV (insertional activity)
1mV (recruitment pattern analysis)

92
Q

_____ is the time required for an electrical stimulus to initiate an evoked potential.
For sensory, means;
For motor, Means:

A

onset latency

sensory: reflects conduction along fastest fibers
motors: not the same, due to cushioning effect of NMJ.

93
Q

____ represents latency along the majority of the axons and is measured at peak of waveform amplitude.
Dependent on_____

A

peak latency

- myelination of the nerve (both motor and sensory)

94
Q

between peak and onset latency, which is a better predictor of actual slowing?

A

peak latency, as this represents the initiation of conduction and therefore saltatory conduction which gives a more accurate measure of slowing.

95
Q

Conduction velocity is the speed in which an impulse travels along a nerve and is primarily dependent on _____.

A

the integrity of the myelin sheath

96
Q

How do you calculate CV?
normal in UE:
normal in LE:

A

distance/time
UE: >50meters/sec
LE: >40meters/sec

97
Q 
Conduction velocity variations with age: 
Newborn: 
1 year: 
3-5 years: 
5th decade:
A

newborn: 50% of that of an adult
1 year: 80%
3-5 years: equal to adult
at 5th decade, CV decreases by 1-2 m/sec per decade

due to segmental demyelination/remyelination and large fiber loss associated with normal aging.

98
Q

conduction velocity decreases ______ per 1 degree dropped.

A

2.4m/sec per 1 degree dropped.

also a 5% decrease in CV has been described for each 1C drop below 29C

99
Q

____ is the maximum voltage difference between two points. Reflects the number of nerve fibers activated and their synchronicity of firing.

A

amplitude

recordings are measured as peak-to-peak or baseline-to-peak.

100
Q

____ is measured from initial deflection from baseline to final return

A

duration. depends on summation and rate of firing of numerous axons

101
Q

___ is a function of both the amplitude and duration of the waveform

A

area.

102
Q

____ reflects the range of conduction velocities of the fastest and slowest nerve fibers.

A

temporal dispersion

seen as a spreading out of the waveform with proximal compared to distal stimulation. due to slower fiber conduction reaching the recording electrode later than faster fibers. No seen with distal stimulation when slow and fast fibers reach recording electrode at relatively the same time. area under the curve essentially is constant.

103
Q

why is a decrease of 50% in SNAP and 15% in MUAP acceptible in CV

A

due t o phase cancellation (page 360)

104
Q

SNAP vs CMAP: which is more sensitive in detecting incomplete peripheral nerve injury?

A

SNAP

105
Q

three benefits of antidromic studies:

sensory n studies

A
  1. easier to record a response than orthodromic studies
  2. may be more comfortable due to less stimulation required.
  3. May have larger amplitudes due to nerve being more superficial at the distal recording sites
106
Q

Recording electrodes in sensory N NCS should be ____ apart. Less than this will alter the waveform how?

A

at least 4cm apart.

If not: 
Peak latency: decreased
Amplitude: decreased
Duration: decreased
Rise time: decreased
107
Q

why are CMAPs unable to differentiate pre and post ganglionic lesions?

A

cell body is located in spinal cord

It can be abnormal with normal SNAPs if the lesion is proximal to the DRG or affecting a purely motor nerve

108
Q

in NCS, in what scenarios would a CMAP be abnormal and a SNAP be normal?

A
  1. Pre-ganglionic sensory n lesion (proximal to DRG)

2. pure motor nerve lesion

109
Q

A CMAP should have an initial negative deflection. If not, it may be due to what 3 things?

A
  1. inappropriate placement of the active electrode from motor point
  2. Volume conduction from other muscles or nerves
  3. anomalous innervations.
110
Q

SNAP vs CMAP:
Pertinent latences:
Amplitude measurements

A

SNAP:
Latency Peak or onset
Amplitude peak to peak

CMAP:
Onset latency (saltatory conduction)
Amplitude baseline to peak.

111
Q
  1. what is an H reflex?
  2. How is it performed?
  3. Activates: ___
  4. Response?
  5. potentiated by?
  6. Abolished by?
A
  1. NCS late response which is electrically-evoked analogue to a monosynaptic reflex
  2. submaximal stimulus at a long duration (0.5-1.0milliseconds)
  3. activated IA afferent nerve fibers
  4. causing an orthodromic sensory response to the spinal cord and an orthodromic motor response back to the recording electrode
  5. potentiated by agonist muscle contraction
  6. abolished by antagonist contraction or increased stimulation causing collision blocking

the morphology and latency remain constant with each stimulation at the appropriate intensity

The mean of ten F-waves can be used as a surrogate for one H-relex.

112
Q

What is the function of a H-reflex?

When is it used?

A

reflects the response of a proximally traveling evoked potential. It is typically used to monitor for S1 radiculopathy in lower extremity or C7 radiculopathy in the upper extremity

113
Q

What is the formula for H-reflex?

A

H-reflex = (9.14 + 0.46) + 0.1(age)

leg length in CM from medial malleolus to popliteal fossa

114
Q

Normal latency for H-reflex?
Side to side difference of ____ is significant.
Above 60 years? _____.

A

28-30milliseconds
>0.5-1.0 milliseconds is significant
add 1.8 milliseconds.

115
Q

What are the two locations generally used for H-reflex

A

S1 pathway: soleus muscle (tibial n)

C7 pathway: flexor carpi radialis (median n)

116
Q

This waveform can be seen in all nerves of adults with UMN (corticospinal tract) lesion as well as in normal infants. It can be normal with incomplete lesions. Once abnormal, its always abnormla.

A

H-reflex

117
Q
  1. What is a F-wave?
  2. How is it produced?
  3. Response?
A
  1. a small late motor response occurring after a CMAP. It represents a late response from approx 1-5% of CMAP amplitude.
  2. short duration, supramaximal stimulation
  3. initiates antidromic motor response to the anterior horn cells in the spinal cord which in turn produces an orthodromic motor response

The f wave is a pure motor response and does not represent a true reflex because there is no synapse along the nerve pathway being stimulated.

118
Q

How is F-wave helpful?

A

polyneuropathies and plexopathies but not overly useful in radiculopathies

119
Q 
Normal latency for F-wave:
-Upper limb: 
-Lower limb
Side to side difference
Location:
A

Upper: 28milliseconds
Lower: 56 milliseconds

side to side difference 2.0 in upper, 4.0 in lower is significant
Location: any muscle

120
Q

___ is a response which can be evoked by a submaximal stimulation and abolished with a supramaximal level ( in CMAP study). Stimulus can travel antidromically along the motor nerve and becomes diverted along a neural branch formed by collateral sprouting due to a previous denervation and reinnervation process.

A

A-(axon) wave - typically occurs between the CMAP and F-wave at constant latency.

121
Q

What is the function of an A(axon)-wave

A

represents collateral sprouting following nerve damage. seen when performing CMAP.

122
Q
  1. What is the Blink reflex?
  2. Initiated by?
  3. Response?

Muscle and N involved?

A
  1. the electrically evoked analogue to the corneal reflex
  2. initiated by stimulating the supraorbital branch of the trigeminal nerve.
  3. Response propagates into the pons and branches to the lateral medulla. Then branches to innervate the ipsalateral and contralateral orbicularis oculi via the facial N.

Two responses are evaluated.
R1: ipsilateral
R2: bilateral - blink is associated with this one.

123
Q 
Blink Reflex pathways: 
Afferent: 
Efferent: 
R1 (early) course: 
R2 (late)course:
A

A: sensory branches of CNV (supraorbital)
E: motor of CN VII (facial)
R1: through pons
R2 through pons and lateral medulla.

124
Q

In blink reflex pathways:
R1 affected by lesions of; (3)
R2 affected by: (6)

A

R1: trigeminal nerve, pons, facial nerve
R2: Consciousness level, parkinsons disease, lateral medullary syndrome, contralateral hemisphere, valium, habituation

125
Q

Normal latency for blink reflex:
R1
R2 ipsilateral (direct)
R3 contralateral (consensual)

A

R1 <41 milliseconds

126
Q

Describe method for direct facial n study:
Stimulated:
Response recorded:

A

Stimulating distal to the stylomastoid foramen at the angle of the mandible
Response recorded over the nasalis muscle. Reference on bridge of nose.

127
Q

_____ is an aberrant regeneration of axons which can occur with facial nerve injuries leading to reinervation of inappropriate muscles. This may present as;

A

Synkinesis.

Presents as lip twitching when closing an eye or crocodile tears when chewing.

128
Q

Direct facial nerve study (NCS) used in what diseases: 7

A
  1. bell’s palsy
  2. neoplasms
  3. fractures
  4. middle ear infections
  5. diabetes mellitus
  6. mumps
    7 lyme disease

stroke?

129
Q

In direct facial N study, what indicates a poor prognosis?

A

absence of an evoked potential in 7 days.

This can be monitored periodically over 2 weeks to assess prognosis. Better outcomes are anticipated for demyelinating vs axonal injuries.

130
Q

Prognosis of Facial N recovery with direct nerve study (NCS)

  1. CMAP less than 10% amplitude of unaffected side:
  2. CMAP 10%-30% of unaffected side
  3. CMAP >30% amplitude of unaffected side
A
  1. poor outcome. Recovery >1 year to incomplete
  2. Fair prognosis. Recovery within 2-8 months
  3. Good prognosis. Recovery within 2 months.
131
Q

What are three interventions for facial N injury?

A

prednisone
massage
e-stim

132
Q

_____ evaluates a time-locked response of the nervous system to an external stimulus. Represents function of an ascending sensory pathway using an afferent potential, which travels from the peripheral N to the plexus, root, spinal cord (posterior column), contralateral medial lemniscus, thalamus, to the somatosensory cortex.

A

Somatosensory evoked potentials (SSEP)

133
Q
  1. What is a somatosensory evoked potential?
  2. initiated by?
  3. Recorded where?
  4. Nerves most commonly used? (2)
A
  1. represents function of the ascending sensory pathways using afferent potential.
  2. repetitive submaximal stimulation of a sensory nerve, mixed nerve, dermatome
  3. recorded from spine or scalp
  4. Upper limb: median n. Lower limb: tibial n.
134
Q

What three problems does a somatosensory evoked potential (SSEP) evaluate for?

A

a. peripheral n injuries
b. CNS lesions such as MS
c. intra-operative monitoring of spinal surgery.

changes in MS are seen 90% of time with the lower limb more likely to be abnormal than the upper limb. ***the most common abnormality is the prolonged interpeak latencies.

135
Q

Which spinal cord pathway is utilized in somatosensory evoked potentials?

A

posterior columns, contralateral medial lemniscus

136
Q

Advantages of SSEP (somatosensory evoked potentials?)

3

A
  1. theoretically evaluates sensory components of peripheral and central nervous system
  2. can aid in studying disorders of CNS (brian, brainstem, SC) as well as dorsal nerve roots and peripheral nerves where severe peripheral disease is noted.
  3. abnormal results are present immediately.
137
Q

Limitations of SSEP (somatosensory evoked potentials)?

A
  1. on evaluates nerve fibers sensing vibration and proprioception
  2. Limited in ability to localize a nerve lesion to a focal area. evals long neural pathway, which may dilute focal lesions and hinder specificity of injury location.
  3. can be adversely affected by sleep, and high doses of general anesthetics (halothane, enflurane, isoflurane)
138
Q

SSEP can be adversely affected by sleep, and high doses of general anesthetics.

  1. Which three GA?
  2. avoided with what? (2)
A
  1. halothane, enflurane, isoflurane

2. nitrous oxide or low dose isoflurane.

139
Q

The most common abnormality in SSEPis?

A

prolonged interpeak latencies

140
Q

Recording sites for SSEP
upper:
lower:

A

upper: erbs point, roots, cervical medullary junction (nucleus cuneatus) and cortical
lower: popliteal fossa, third lumbar, T12/LS spine, cortical

141
Q

duration of insertional activity: (plus etiology)
Normal:
Increased:
Decreased:

A

N: 300ms - muscle depolarization
I: >300-500ms - denervation/irritable cell membrane
D: <300ms - fat, fibrosis, edema, electrolyte abnormalities.

142
Q

two types of normal spontaneous activity at rest:

A
  1. miniature endplate potentials (MEPP) due to spontaneous quanta release (100-200 quanta) which occurs every 5 seconds. Results in 10-50uV, nonpropogated potential seen on the screen. MONOPHASIC
  2. endplate potentials (EPP) endplate spike due to increased Ach release, provoked by needle irritation of the muscle fiber or synchronization of several MEPPs BIPHASIC

occurs if placed near a NMJ/endplate.

143
Q

spontaneous waveform generated by multiple muscle fibers will looks like:

A

complex repetitive discharges

144
Q

spontaneous waveform generated by terminal axon will look like

A

end plate spikes

145
Q

spontaneous waveform generated by motor neuron/axon will look like (5)

A

fasciculation, myokymia, tetany, cramp, neuromyotonia

146
Q

spontaneous waveform generated by NMJ looks like

A

end-plate noise

147
Q

abnormal spontaneous waveform generated by muscle fibers looks like (4)

A

fibrillation, positive sharp waves, myotonia, complex repetitive discharges

148
Q

_____ are spontaneously firing action potentials originating from denervated single muscle fibers, secondary to uncontrolled ACh release. hallmark sign is regularity of firing.

A

fibrillation potentials (abnormal activity generated from muscle fibers)

“rain on a tin roof”

149
Q

_____ are needle recordings of an action potential of a single muscle fiber. There is propagation to, but not past, the needle tip. This inhibits the display of the negative deflection of the wave form.

A

positive sharp waves (PSW)

“Dull thud or chug”

150
Q

____ are “bizarre high frequency discharges” which are polyphasic/serrated action potentials originating from a principle pacemaker, initiating a group of single muscle fibers to fire in near synchrony.

A

complex repetitive discharges (CRD)

“motor boat”

151
Q

____ results from a process in which denervated muscle fibers are reinnervated by collateral sprouting from axons of a neughboring motor unit.

A

complex repetitive discharges (CRD)

152
Q

what is the hallmark sign of complex repetitive discharges?

A

regular interval between each discharge and within each discharge.

153
Q

_____ are biphasic single muscle fiber action potentials triggered by needle movement, percusion, or voluntary contraction. caused by an alteration of the ion channels in the muscle membrane

A

myotonic discharges. can be seen with or without clinical myotonia.

sounds like “dive bomber”

154
Q

What is the hallmark sign of myotonic discharge?

A

smooth change in rate and amplitude.

155
Q

Abnormal spontaneous activity generated from motor UNIT (neural source)

A

fasciculations, neuromyotonic discharges, cramp discharges, artifact potentials

156
Q

____ are spontaneous discharges originating from any portion of a single motor unit and result in intermittent muscle fiber contraction.

A

fasciculations

if associated with fib or PSW, considered to be pathological.

hallmark, irregular firing motor unit.

157
Q

_____ are groups of MUAPs firing repetitively. Hallmark is semi-regularity between each discharge and within each discharge

A

myokymic discharges.

“marching soldiers”

158
Q

MS, brainstem neoplasm, polyradiculopathy, bells palsy, radiation plexopathy, compression neuropathy, rattlesnake venom may all present as ______on spontanous activity

A

myokymic discharges; facial myokymia; extremity myokymia

159
Q

____ is a disorder associated with continuous muscle fiber activity resulting in the appearance of muscle rippling and stiffness secondary to irritable nerves.

Discharges seen with it?

A

Isaac’s syndrorme

Neuromyotonic discharges - originating from motor axons. The progressive decrement of its waveform is due to individual muscle fiber fatigue and drop off.

160
Q

___ are discharges associated with involuntary repetitive firing of MUAPs in a large area of muscle. Usually associated with painful muscle contraction and are synchronous.

A

cramp discharges.

examples: salt depletion, uremia, pregnancy, myxedema, prolonged muscle contraction, myotonia congenita, myotonic dystrophy, stiff-man’s syndrome.

161
Q

Amplitude is measured by:
Increased by:
Decreased by:
Normal:

A

most negative peak to most positive peak.
reinnervation process
loss of muscle fibers
1mV

162
Q

Rise time measured by:
Represents;
normal:

A

baseline to peak of negative wave
proximity of needle to motor unit.
<500us

163
Q 
Duration measured by: 
Represents: 
Increases with: 
decreases with: 
Normal:
A

initial departure from baseline to return
# of muscle fibers within the motor unit
Increases (>15msec) as the motor unit territory increases from collateral sprouting
Decreases (<5msec) with loss of muscle fibers.
Normal: 5-15msec.

164
Q

Define “turns” on MUAP

A

changes in direction of the wave without crossing the baseline. Also known as serrations.

165
Q

Phases calculated by:
Represents:
What is polyphasicity?
Normal:

A

number of times the wave crosses baseline plus 1
synchronicity of muscle fiber action potentials firing
>5 crossings
Normal 2-4

166
Q

what are causes of polyphasicity of MUAP?

A
  1. muscle fiber dropout
  2. alterations in fiber conduction velocity
  3. reinnervation from collateral sprouting.

Normal 15% (concentric needle) or 30% (monopolar needle)
More frequent in the elderly.

167
Q

What differentiates myopathic from neuropathic process

A

recruitment pattern.

168
Q

Unstable potentials are seen most commonly in what disorders

A

NMJ disorders due to blocking of the discharges. Can also be seen in motor neuron disorders, neuropathic disorders, muscle trauma and reinnervation.

169
Q

____ are small potentials originating from a few muscle fibers. Time locked to occur approximately 10-15msec after a MUAP.

Causes?

A

satellite potentials

incomplete myelin formation and immature terminal sprouts from chronic reinnerva`tion or a myopathy.

170
Q

_____ refers to two or more MUAPs firing recurrently and together in a semirhythmic fashion.

seen in? 5

A

doublet/multiplet potentials

ischemia, hyperventilation, tetany, motor neuron disease, metabolic disorders

171
Q

____ refers to the extremely large MUAPs (>5mV)

Seen in?

A

Giant potentials
Poliomelitis
AKA large amplitude potentials

172
Q

Reduced recruitment is often seen in which conditions?

A

neuropathic (can also be due to any disorder which destroys or blocks axonal conduction or muscle fibers.

173
Q

Early recruitment is most commonly seen in which conditions?

A

myopathic conditions (results in loss of muscle fibers, causing less force to be generated per motor unit, thus more motor units must be called upon)

174
Q

Define Firing rate:

How is it calculated

A

the # of times a MUAP fires per second
measured in Hertz (Hz)
Calculated by dividing 1000 by the interspike interval (II) measured in milliseconds

175
Q

Define recruitment frequency:

Normal?>

A

This is the firing rate of the first MUAP when a second MUAP begins to fire. Initiated by an increase in the force of a contraction.
Normal < or = 20Hz.
Above this, neuropathic process

176
Q

define recruitment interval:

A

This is the interspike interval (in milliseconds) between two discharges of the same MUAP when a second MUAP begins to fire. It is initiated by an increase in the force of a contraction. Normal is considered to be 100ms

177
Q

Recruitment ratio represents:

How is it calculated?

A

represents recruitment capabilities, especially when a patient demonstrates difficulty in controlling a contractile force.
Calculated by dividing firing ratio of the first MUAP by the number of different MUAPs on the screen.

RR = FR/# different MUAPs.

178
Q

_____ is the ability of a motor unit to fire faster to produce a greater contractile force and is controlled by a central process.

A

Activation

179
Q

_____ is a qualitative or quantitative description of the sequential appearance of MUAPs. It is the electrical activity recorded from a muscle during a maximum voluntary contraction. Comprised of recruitment and activation

A

interference pattern.

180
Q

What if a patient is asked to generate a force and only a few MUAPs are seen while the Hz continues to remain low?

A

indicative of decreased activation from poor patient cooperation and is not a result of abnormal recruitment.

CUCC (26 decks)

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