CNP Course - NCS Flashcards

1
Q

Median Motor muscle

A

APB

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2
Q

Median motor G1 site

A

APB 1/3 from wrist

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3
Q

Median motor distal stim site

A

wrist, b/w FCR and palmaris longus

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4
Q

median motor proximal stim site

A

elbow, over brachial pulse

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5
Q

median motor distance from G1

A

7cm

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6
Q

ulnar motor muscle

A

ADM

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7
Q

ulnar motor G1 site

A

1/2 from origin

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8
Q

ulnar motor distal stim site

A

volar wrist, radial to FCU

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9
Q

ulnar motor proximal stim site

A

5cm distal to medial epicondyle
5cm proximal to medial epicondyle

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10
Q

ulnar motor distance from G1

A

6.5cm

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11
Q

peroneal motor muscle

A

EDB

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12
Q

peroneal motor G1 site

A

mid EDB muscle

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13
Q

peroneal motor distal stim site

A

ant ankle lat to TA

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14
Q

peroneal motor proximal stim site

A

behind knee

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15
Q

peroneal motor distance from G1

A

8.5cm

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16
Q

tibial motor muscle

A

AH

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17
Q

tibial motor G1 site

A

1cm below/behind navicular

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18
Q

tibial motor distal stim site

A

1-2cm behind/above medial malleolus

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19
Q

tibial motor proximal stim site

A

popliteal fossa

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20
Q

tibial motor distance from G1

A

8cm

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21
Q

blink motor muscle

A

orb oculi

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22
Q

blink motor G1 site

A

on line with pupil

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23
Q

blink motor G2 site

A

lateral palpebral fissure

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24
Q

blink motor stim site

A

supraorbital notch

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25
Q

blink motor distance from G1

A

no standard distance

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26
Q

facial motor muscle

A

nasalis

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27
Q

facial motor G1 site

A

1cm above nares

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28
Q

facial motor G2 site

A

same on opposite side

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29
Q

facial motor stim site

A

below lobe, ant/low mastoid

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30
Q

facial motor distance from G1

A

no standard distance

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31
Q

median anti G1 site

A

ring D2 proximal phalanx

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32
Q

median anti G2 site

A

3.5-4cm distal to G1

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33
Q

median anti distal stim site

A

b/w FCR and PL volar wrist

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34
Q

median anti proximal stim site

A

elbow over brachial pulse

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35
Q

median anti distance

A

13cm

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36
Q

ulnar anti G1 placement

A

ring D5 proximal phalanx

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37
Q

ulnar anti G2 site

A

3.5-4cm distal to G1

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38
Q

ulnar anti distal stim site

A

volar wrist, radial to FCU

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39
Q

ulnar anti proximal stim site

A

5cm proximal to medial epicondyle

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40
Q

ulnar anti distance

A

11cm

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41
Q

median ortho/palmar G1 site

A

distal: wrist
proximal: block over nerve at elbow

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42
Q

median ortho/palmar G2 site

A

3.5-4cm distal to G1

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43
Q

median ortho/palmar stim site

A

thenar crease 2nd MC

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44
Q

median ortho/palmar distance

A

8cm

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45
Q

ulnar ortho/palmar G1 site

A

distal: wrist
proximal: block over nerve at elbow, 5cm proximal to medial epicondyle

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46
Q

ulnar ortho/palmar G2 site

A

3.5-4cm distal to G1

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47
Q

ulnar ortho/palmar stim site

A

hypothenar crease 4th MC

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48
Q

ulnar ortho/palmar distance

A

8cm

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49
Q

radial sensory G1 site

A

on nerve over EPL

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50
Q

radial sensory G2 site

A

4cm distal to G1 on 2nd MC/FDI

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51
Q

radial sensory distal stim site

A

2/3 forearm, dorsal radius

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52
Q

radial sensory proximal stim site

A

elbow b/w lat biceps hooked under brachioradialis

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53
Q

radial sensory distance

A

10cm

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54
Q

superficial peroneal sensory G1 site

A

3cm proximal to 1/2 line between lateral malleolus and AT tendon

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55
Q

superficial peroneal sensory G2 site

A

3.5-4cm distal to G1

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56
Q

superficial peroneal sensory stim site

A

anterolateral fibula

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57
Q

superficial peroneal sensory distance

A

14cm

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58
Q

sural G1 site

A

behind lateral malleolus

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59
Q

sural G2 site

A

3.5-4cm distal to G1, below lateral malleolus

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60
Q

sural stim site

A

point A, B, C, all post 1-3cm lateral to midline

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61
Q

sural distance

A

A- 7cm, B- 14cm, C- 21cm

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62
Q

medial plantar G1 site

A

block 1cm proximal to medial malleolus over artery

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63
Q

medial plantar stim site

A

med plantar fascia, 2cm distal to navicular tubercle

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64
Q

medial plantar distance

A

12-14cm

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65
Q

lateral plantar distance

A

block 1cm proximal to medial malleolus over artery

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66
Q

lateral plantar stim site

A

2.5-3cm lateral to stim site of medial plantar

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67
Q

lateral plantar distance

A

14-16cm

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68
Q

why perform motor NCS

A

objective evidence of neuromuscular disease (weakness)
localization of focal nerve lesion (ulnar neuropathy)
identify subclinical involvement (neuropathy in arms)
assess NMJ
pathophysiology (axonal vs demyelinating)
follow response to treatment (“summated CMAP”)

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69
Q

cathode does what

A

negatively charged and depolarizes the axon

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70
Q

anode does what

A

positively charged and hyperpolarizes axon

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71
Q

reversal of cathode-anode can cause

A

inaccurate distance measurement (error of 3cm may be made)
anode block
prolonged distal latency

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72
Q

difficulty in nerve localization situations

A

unfamiliar with anatomy
limb edema
post-trauma or surgery
large body habitus
common sites: elbow, radial nerve, Erb’s point

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73
Q

effect from difficulty in nerve localization

A

submaximal stimulation
higher stimulus intensity -> current spread to other nerves, increased discomfort

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74
Q

what is the technique used to optimally localize the nerve being tested?

A

sliding

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75
Q

understimulation (submaximal stimulation)

A

number of conducting fibers is underestimated
larger, faster conducting fibers not depolarized
result: falsely low amplitude, falsely prolonged distal latency, falsely slowed conduction velocity, non-reproducible response

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76
Q

minimize understimulation by

A

observe waveform
increase intensity: 10% > maximal
reduce impedence
increase cathode-anode separation

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77
Q

acceptable reduction in amplitude and area between distal and proximal sites

A

<20% reduction in amplitude and area

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78
Q

if waveforms dissimilar, think of

A

understimulation
overstimulation
stimulation of adjacent nerves at one site and not the other
anomalous connections between nerves
temporal dispersion

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79
Q

common uses of arm motor NCS

A

upper extremity mononeuropathy (CTS, ulnar neuropathy)
arm pain (cervical radiculopathy)
brachial plexopathy
peripheral neuropathy
myopathy
NMJ disorder
motor neuron disease

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80
Q

short segment incremental stimulation

A

inching study
way to assess focal nerve segments (e.g. focal ulnar neuropathy)
short, segmental stimulation
each stimulus site separated by the width of the stimulator (approx 2cm)
begin at distal site (higher amplitude response) and move proximal

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81
Q

focal nerve compression - neuropraxia

A

current must spread over several nodes
longer time to reach threshold at each node
conduction velocity slowed across compression
blocking of conduction through the abnormal area
differential slowing of conduction in some axons resulting in dispersion

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82
Q

situations of neuropraxia

A

cool
ischemia
local anesthetic
compression

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83
Q

NCS errors

A

inaccurate measurement of nerve length
wrong distal distance
initial positive CMAP deflection
different form or size of the CMAP at the two sites of stimulation
cool limb temp

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84
Q

inaccurate measurement of nerve length correction

A

tape measure follow course of nerve

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85
Q

wrong distal distance correction

A

accurately measure before and after stimulation

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86
Q

initial positive CMAP deflection correction

A

move G1 electrode
ensure not overstimulation or stimulator near ulnar nerve

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87
Q

different form or size of the CMAP at the two sites of stimulation correction

A

check for submaximal stimulation at elbow

88
Q

failure to localize nerve correction

A

sliding

89
Q

cool limb temperature correction

A

monitor continuously and warm limb

90
Q

musculocutaneous uses

A

musculocutaneous mononeuropathy
upper trunk plexopathy
multifocal motor neuropathy
peripheral neuropathy (absent distal responses)
NMJ disorders (repetitive stimulation)

91
Q

radial EDC uses

A

radial neuropathy
wrist drop
posterior cord plexopathy
multifocal motor neuropathy

92
Q

radial motor muscle

A

EDC

93
Q

radial motor G1 site

A

middle of EDC on dorsum of forearm

94
Q

radial motor distal stim site

A

bw biceps tendon and brachioradialis

95
Q

radial motor proximal stim site

A

lateral border of triceps at deltoid insertion

96
Q

radial motor distance

A

10cm distal to lateral epicondyle

97
Q

musculocutaneous motor G1 site

A

1/2 distance between tendons of origin and insertion of biceps over center of muscle belly

98
Q

musculocutaneous distal stim site

A

under biceps tendon

99
Q

musculocutaneous proximal stim site

A

Erb’s point

100
Q

axillary motor uses

A

axillary mononeuropathy
upper trunk, posterior cord plexopathy
NMJ disorder (repetitive stimulation)

101
Q

axillary G1 site

A

1/2 distance b/w acromium and along a line which bisects the deltoid, insertion of the deltoid

102
Q

axillary distal stim site

A

Erb’s point

103
Q

suprascapular uses

A

suprascapular neuropathy
upper trunk plexopathy

104
Q

suprascapular G1 site

A

2cm below scapular spine, midway b/w medial border of scapula and acromium

105
Q

utility of sensory NCS

A

objective evidence of sensory loss
most sensitive studies in polyneuropathies and mononeuropathies
identify subclinical sensory involvement (e.g. myopathy)
pre-ganglionic vs post-ganglionic injury
testing a pure sensory nerve
children

106
Q

SNAPs

A

generator: summated action potentials of large demyelinated and unmyelinated sensory axons (DRG and distal)
greater range of diameters than motor axons. produces normal “dispersion” of sensory response over distance

107
Q

SNAP amplitude

A

reflect number of conducting axons
much lower than motor amplitudes - more noise and artifact interference
responses much lower (>50%) with proximal stimulation vs distal (normal dispersion) - due to “phase cancellation”

108
Q

SNAP conduction velocity

A

faster (by 3-6m/s) than motor axons
faster in proximal nerves segments than distal
increases until age 5 years and decreases after age 30

109
Q

shock artifact reduced by

A

skin prep - abrade and clean
ground
minimize paste
minimal intensity and duration
slide
orientation - ‘rotate’

110
Q

averaging sensory NCS

A

useful for defining very small responses
improves signal to noise ratio
- should not be used as the sole technique to eliminate noise
normally average 3-5 responses

111
Q

correct motor artifact

A

ensure electrodes away from metacarpal-phalangeal joint
wrap gauze around ring electrodes

112
Q

temperature effects on NCS

A

cool temp:
- increases amplitude
- slows CV
- prolongs distal latency

113
Q

onset latency

A

used when measuring conduction velocity in SNAPs

114
Q

peak latency

A

used when measuring distal latency in SNAPs

115
Q

recording errors in sensory NCS

A

inadequate skin prep
wrong location
plugged in wrong
electrodes not plugged into the preamplifier

116
Q

median sensory NCS uses

A

carpal tunnel syndrome
median mononeuropathy
polyneuropathy
cervical radiculopathy (should be normal)
brachial plexopathy

117
Q

ulnar sensory uses

A

ulnar neuropathy
polyneuropathy
polyradiculopathy
cervical radiculopathy (should be normal)
brachial plexopathy

118
Q

radial sensory uses

A

radial neuropathy
cervical radiculopathy (should be normal)
brachial plexopathy (upper trunk, posterior cord)
polyneuropathy (esp when superimposed possible CTS and ulnar neuropathy)
polyradiculopathy

119
Q

lateral antebrachial cutaneous uses

A

musculocutaneous neuropathy
brachial plexopathy (upper trunk, lateral cord)

120
Q

medial antebrachial cutaneous uses

A

brachial plexopathy (lower trunk, medial cord)
C8-T1 radiculopathy (should be normal)
ulnar neuropathy (should be normal)

121
Q

pitfalls of sensory NCS

A

technically more difficult than motors
more prone to artifact, noise
very low amplitudes

122
Q

why perform leg NCS

A

leg pain (radiculopathy)
peripheral neuropathy (length-dependent)
lower extremity mononeuropathy (e.g. fibular)
polyradiculopathy
NMJ disorders
myopathy
motor neuron disease

123
Q

limitations of LE NCS

A

relatively few nerves to stimulate in leg
interpreting absent sensory responses - may be normal in individuals >60yo
few reliable nerves to test upper lumbar levels - most assess L4-S1
local muscle factors may affect NCS (e.g. repetitive foot trauma, foot surgery)

124
Q

fibular motor uses

A

peripheral neuropathy
lumbosacral radiculopathy (L5)
lumbosacral plexopathy
sciatic neuropathy
fibular mononeuropathy
motor neuron disease
NMJ disorder (EDB rarely helpful)
myopathy (rarely helpful)

125
Q

if amplitude at knee is larger than ankle for fibular motor

A

check for understimulation at the ankle
check for overstimulation at the knee
stimulus behind the lateral malleolus (accessory fibular nerve)

126
Q

fibular f-waves…

A

often absent, even on normal patients

127
Q

superficial fibular sensory uses

A

peripheral neuropathy
lumbosacral radiculopathy (L5) - usually normal, may be abnormal
lumbosacral plexopathy
sciatic neuropathy
fibular mononeuropathy

128
Q

superficial fibular sensory G1 site

A

3cm proximal to midpoint bimalleolar line, between lateral malleolus and AT tendon

129
Q

superficial fibular sensory stim site

A

over superficial fibular nerve on lateral calf just anterior to fibula

130
Q

superficial fibular sensory distance

A

14cm

131
Q

tibial motor uses

A

peripheral neuropathy
polyradiculoneuropathy
lumbosacral radiculopathy (S1)
lumbosacral plexopathy
sciatic neuropathy
tibial mononeuropathy
motor neuron disease

132
Q

tibial motor accepted amplitude reduction

A

up to 50% amplitude reduction from ankle to knee

133
Q

medial and lateral plantar sensory uses

A

peripheral neuropathy
polyradiculoneuropathy
lumbosacral radiculopathy
lumbosacral plexopathy
sciatic neuropathy
tibial mononeuropathy

134
Q

tibial H reflex uses

A

S1 radiculopathy
Lumbosacral plexopathy
sciatic neuropathy

135
Q

what is H reflex

A

stimulate Ia afferent fibers (sensory)
- action potential propagates orthodromically
- at cord, few AHCs depolarize
- action potential down motor axons
electrophysiologic correlate of “achilles” reflex

136
Q

how to perform H reflex

A

selectively stimulate sensory fibers by:
- low stimulus intensity
- higher stimulus duration

137
Q

H reflex errors

A

cathode distal
not over fascicle of nerve with IA afferents
stimulation at too rapid a rate
stimulation of both the peroneal and tibial together
different distances on the two sides
measurement of a response that is lower amplitude than the M-wave which may be an F-wave

138
Q

sural sensory uses

A

peripheral neuropathy
polyradiculoneuropathy
lumbosacral radiculopathy (normal)
lumbosacral plexopathy
sciatic neuropathy
tibial mononeuropathy

139
Q

femoral motor uses

A

upper lumbar radiculopathy (normal)
lumbosacral plexopathy
femoral neuropathy
NMJ disorder (e.g. LEMS)

140
Q

femoral motor G1 site

A

over the center of the rectus femoris, 1/2 way between the inguinal ligament and patella

141
Q

femoral motor stim

A

monopolar surface prong
single prong held in the femoral triangle, just lateral to femoral pulse, may have to be pushed deep into the tissue

142
Q

saphenous sensory uses

A

upper lumbar radiculopathy (normal)
lumbosacral plexopathy
femoral neuropathy

143
Q

why assess proximal nerves or roots?

A

proximal mononeuropathies
radiculopathies
polyradiculopathy
brachial plexopathy
cranial neuropathies
NMJ disorders

144
Q

techniques available to assess proximal nerves

A

routine motor NCS - late responses
- F waves and H reflex
proximal nerve stimulation
- plexus or root stimulation
needle EMG of proximal muscles
- indirect assessment of nerve
somatosensory evoked potentials

145
Q

F waves

A

motor axon stimulation
axon potential travels in both directions = M and F waves
each stimulus activates few AHC
multiple stimuli usually results in activation of different motor neurons

146
Q

F-waves morphology

A

vary in latency and morphology
Jendrassik maneuver may enhance activation
percentage varies with the nerve (least with peroneal)

147
Q

F wave errors

A

poor relaxation: background activity interrupts the baseilne
axon reflex: stable and reproducible
delated M wave component: stable response. the temporal relationship to the M wave is fixed with proximal or distal movement of the stimulating electrode

148
Q

axon reflex - A wave

A

motor stimulation - action potential propagates antidromically toward AHC, but loops through a collateral sprout and returns orthodromically to muscle

149
Q

H wave vs. F wave

A

H wave:
- high amplitude (mV)
- less variable
- maximal amplitude with submaximal stimulation
- blocked by maximal stimulation (by antidromic activation of motor axons)
F wave:
- low ampiltude (uV)
- variable morphology
- maximum amplitude with supramaximal stimulation
- not blocked with maximal stimulation

150
Q

form of direct proximal nerve stimulation

A

Erb’s point

151
Q

Erb’s point

A

supraclavicular fossa: 1/2 distance from acromium to sternum
requires pressure
rotate to direct current spread

152
Q

criteria for abnormality at Erb’s point stimulation

A

low amplitude or no response
amplitude reduction from upper arm site
- ulnar/hypothenar >20% (or >10m/s slowing of CV)
- musculocutaneous/biceps >20%

153
Q

pitfalls of erb’s point

A

cannot completely isolate single trunk/cord of plexus
stimulates multiple “nerves” therefore record volume conducted responses
selectively record from “isolated” muscles
- ulnar, musculocutaneous, axillary, radial
ensure supramaximal stimulation
ensure proper location of electrode (slide)

154
Q

why perform repetitive stim

A

suspect NMJ disorder (MG, LEMS)
nonspecific weakness’
exclude myasthenia gravis in patient with fatigue, dysarthria, diplopia
pre-synaptic vs post-synaptic
children

155
Q

NMJ physiology

A
  1. action potential
  2. Ca2+ channels open
  3. synaptic vesicles released
  4. ACh binds receptor
  5. sodium channels open
  6. sodium influx
  7. generation of end plate potential
  8. muscle fiber contraction
156
Q

factors that determine MEPP (and EPP) size

A

number of ACh molecules per quanta
structure of synapse
number and function of AChR
number and function of AChE

157
Q

repetitive stimulation does what to safety factor

A

stresses the safety factor
- decrease in number of available ACh quanta
- decrease in number of ACh molecules released
- results in decrease in magnitude of EPP

158
Q

effect of stimulation frequency at slow rates (2-5Hz)

A

less ACh released with the second action potential
maximizes ACh release from immediate store
minimize accumulation of Ca2+ and mobilization of additional ACh
maximum reduction in EPP amplitude by 4-5th response

159
Q

effect of stimulation frequency at fast rates (10-50Hz)

A

amount of ACh released increases
after a series of stimuli (tetanic) the potentiation of ACh release may persist for 30-60 seconds
- maximizes accumulation of Ca2+ and mobilization of additional ACh (transient increase EPP)
- post-activation exhaustion: resynthesis and mobilization of ACh, reset VGCC (2-10 minute duration of very low EPP)

160
Q

normal RNS

A

EPP safety factor is so large that these small change sin EPP amplitude have no effect
each nerve action potential results in a muscle fiber action potential and muscle contraction

161
Q

disorders of neuromuscular transmission if EPP is marginally above threshold

A

slow rates result in lower amplitude EPP
EPP may not reach threshold
neuromuscular transmission may fail
decrease in the number of muscle fibers contracting

162
Q

disorders of neuromuscular transmission if EPP is just below threshold

A

rapid rates result in an increased EPP amplitude
EPP may exceed threshold
increase, or increment, or facilitation of neuromuscular transmission
increment in the number of muscle fibers responding

163
Q

poor RNS technique can result in

A

false negative study
false positive study
excess pain
excess time of the study
frustration

164
Q

RNS technique

A

limb immobilization
supramaximal stimulation with as small a stimulus as possible

165
Q

Distal nerves tested in RNS

A

ulnar and peroneal
(median, anconeus)

166
Q

proximal nerves tested in RNS

A

spinal accessory
(axillary, musculocutaneous, femoral)

167
Q

cranial nerves tested in RNS

A

facial
(trigeminal)

168
Q

brief exercise findings and when to perform

A

if abnormal decrement or low amplitude CMAP - consider LEMS
- patient exercising for 10 secs almost same effect as rapid stim with less discomfort
normal - should improve decrement to a variable degree

169
Q

brief exercise path

A

release of ACh potentiated for 30-60 seconds
- postactivation (post-tetanic) potentiation
- EPP amplitude increased
- evoked CMAP may be markedly increased in the myasthenic syndrome or botulism
- myasthenia gravis the baseline decrement may be decreased or absent

170
Q

when to perform 1 minute exercise

A

if no decrement or only a very questionable decrement on baseline testing
- assess for postexercise exhaustion
- any defect of neuromuscular transmission will be maximized
isometric exercise for 1 minute
after 1 minute of exercise, 4 stimuli are given at 2Hz immediately after exercise, and at 30, 60, 120, 180, and 240 seconds after exercise

171
Q

criteria of abnormality on RNS

A

conservative criteria of abnormality: decrement of at least 10% in 2 different muscle/nerve preparations
- tapering pattern
- repair after exercise
- post exercise exhaustion

172
Q

TRUE decrement

A

baseline testing: reproducible degree
baseline: stable
largest drop: between 1st and 2nd stimulus
pattern of decrement: tapering
following brief exercise: repair

173
Q

FALSE decrement

A

baseline testing: variable decrement
baseline: noisy or variable
largest drop: variable (“roller coaster”)
pattern of decrement: variable
following brief exercise: no repair

174
Q

diseases with decrement

A

neuromuscular junction
- myasthenia gravis, lambert eaton, drugs/toxins
nerve terminal disorders
- progressive MND (e.g. ALS), early reinnervation, polyradiculopathy (GBS)

175
Q

falsely negative RNS

A

low temperatures
successfully treated - AChE inhibitors should be d/c for at least 6-8hrs
patients should be tested when effects of treatments such as PLEX, IVIG, and corticosteroids are minimal

176
Q

technical errors in RNS suspected if

A

results are not reproducible
pattern or envelope of decrement, increment, post exercise potentiation or exhaustion are unusual
baseline shifts
changes in configuration

177
Q

protocol for generalized MG - high suspicion

A

routine motor and sensory NCS
RNS in distribution of weakness - distal and proximal muscles, ulnar, spinal accessory, facial
confirm decrement in 2 muscles
needle EMG: MUP variation

178
Q

protocol for generalized MG: low suspicion

A

fewer RNS, but still in distribution of symptoms
less time spent on exercise unless unexpected results found
possibly - SFEMG if all negative to “prove” no disorder of NMT

179
Q

when to perform 10sec exercise

A

want to assess for facilitation
- abnormal decrement or low amplitude CMAP (? LEMS)
- isometric for 10seconds
- normal or MG should improve decrement slightly

180
Q

when to perform 1min exercise

A

want to assess for exhaustion (worsening decrement)
- isometric exercise for 1 minute
- stimulate at 30, 60, 120, 180, and 240 seconds after exercise

181
Q

presynaptic NMJ disorders

A

decrement similar to postsynaptic disorders
significant increase in CMAP amplitude (facilitation) with 10sec exercise or rapid rates of stimulation (>10Hz)
criteria of abnormality: 200% facilitation or more

182
Q

blink reflex

A

afferent: trigeminal - supraorbital branch, infraorbital branch
synapses:
- ipsilateral pontine sensory nucleus (Vp) - orbic. oculus (R1)
- multisynapses - spinal nucleus of V (pons & medulla) - both orbic oculi (R2)
efferent: facial nerve
- facial nucleus (pons)

183
Q

prolonged latency of R1 and bilateral R2s when stimulating involved side

A

trigeminal nerve lesion
helpful in sensory root lesions of the Vth nerve (tumor, post-herpetic, connective tissue disease)
normal in idiopathic trigeminal neuralgia
infraorbital stim may be useful in lesions involving V2 distribution

184
Q

stimulate affected side, prolonged or absent R1 and R2, contra R2 is normal

A

facial nerve lesion
stimulate normal side, ipsi R1 and ipsi R2 are normal, contra R2 prolonged

185
Q

blink reflexes in peripheral neuropathies

A

may demonstrate prolonged R1 and R2 latencies, demyelinating neuropathies
- AIDP or CIDP
- Charcot Marie Tooth type I, III
may be absent in severe sensory ganglionopathy
- abnormal blink response may favor a nonparaneoplastic etiology

186
Q

utility of facial NCS

A

diagnosis and localization of facial neuropathies (e.g. Bell’s palsy)
assists in prognostication of facial neuropathy
assessment of NMJ disorders (with repetitive stimulation), such as myasthenia gravis

187
Q

potential pitfalls to facial NCS

A

high stimulus intensity required to maximally stimulate facial nerve
volume conduction from overstimulation and masseter response

188
Q

facial NCS prognostic parameters in Bell’s palsy

A

latency
amplitude
threshold excitability

189
Q

latency in facial NCS prognostication of Bell’s Palsy

A

5-7 days.
longer latency (0.6ms longer) with reduced amplitude may develop associated synkinesis

190
Q

amplitude in facial NCS prognostication of Bells palsy

A

<10% of unaffected side, poorer recovery (>6 months, synkinesis)
10-30% recovery between 2-8 months
>30% good prognosis within 3 months

191
Q

threshold excitability in facial NCS prognostication of Bells palsyy

A

using constant current duration of 0.1ms-usually difference between sides <2mA
patients with normal or slightly increased excitability have excellent prognosis
patients w/ difference of 10mA do more poorly
can be used as early as 72 hours

192
Q

differential diagnosis of abnormal facial movements

A

blepharospasm
tics
focal motor seizure
hemifacial spasm
myokymia
synkinesis (from bell’s palsy)

193
Q

hemifacial spasm NCS

A

lateral spread

194
Q

hemifacial spasm EMG

A

bursts (10-200msec) of single or few MUP
variable interval between bursts (20-225ms)
high firing rate within burst (200-300Hz)

195
Q

synkinesis

A

contraction of a muscle, not typically innervated by a nerve or nerve branch, when a muscle supplied by the nerve contracts
results from aberrant reinnervation

196
Q

needle EMG in cranial muscles

A

MUPs usually smaller amplitude and shorter duration
easily accessible muscles
- trigeminal: masseter
- facial n: orb oculi, orb oris, frontalis, mentalis
- spinal accessory: trap, SCM
laryngeal muscles (CNX) can be examined
tongue muscles (hypoglossal nerve) - difficult to relax

197
Q

types of pitfalls in NCS

A

technique-related
physiologic
anomalous anatomy
interpretation

198
Q

identifying technical errors

A

pay close attention to details of technique
close scrutiny of waveforms
don’t only look at numerical data

199
Q

imprecise nerve localization situations

A

unfamiliar with anatomy
limb edema
post-trauma or surgery
large body habitus
common sites: sural, tibial (knee), radial, Erb’s

200
Q

effect of imprecise nerve localiz\ation

A

submaximal stimulation
higher stimulus intensity
- current spread to other nerves
- increased discomfort

201
Q

understimulation

A

submaximal stimulation leads to: underestimate of number of conducting fibers, larger faster conducting fibers not depolarized
results in: falsely low amplitude, falsely prolonged distal latency, falsely slowed conduction velocity, nonreproducible response

202
Q

effect of stimulator pole separation

A

narrow: fewer nerves stimulated, more localized site of stimulation, lower amplitude
wider (monopolar stimulator): more nerves stimulated, more current spread, more spread along nerve

203
Q

overstimulation effects

A

current spread to adjacent nerve -> falsely high amplitude, inaccurate latency and CV measurement
at proximal site -> higher amplitude than distal site, may mimic anomalous anatomy
direct muscle stimulation -> false negative decrement (repetitive stimulation)

204
Q

methods to correct overstimulation

A

small, incremental increase in stimulus intensity (e.g. 5-10mA)
sliding technique
observe muscle contraction
observe waveform morphology for change

205
Q

clues to inappropriate G1 placement motor studies

A

positive initial deflection (all stim sites)
unexpectedly low amplitude
atypical waveform morphology

206
Q

cool temperature pathophysiology

A

ion channels remain open longer -> prolonged action potential, prolonged depolarization of the excitable nerve membrane, prolonged repolarization

207
Q

cool temperature NCS effect

A

slowed conduction velocity
prolonged distal latencies
higher amplitude responses
improves neuromuscular transmission

208
Q

motor artifact

A

may be misinterpreted as sensory response
can interfere with precise measurement on sensory
most commonly seen in antidromic studies

209
Q

correct motor artifact

A

placement of ring electrodes
assess peak latency with G1 movement

210
Q

martin gruber anastomosis

A

basic concept: ulnar fibers travel in median nerve at elbow then ‘cross (back) over’ to ulnar nerve in forearm
- present in up to 30% of forearms (68% bilateral)
one or more muscles involved
- FDI
- adductor policis
- flexor pollicis brevis
- abductor digiti minimi

211
Q

type 1 martin gruber anastomosis

A

ulnar NCS: elbow CMAP >20% lower than wrist, below elbow CMAP similar to AE
median APB: normal results

212
Q

type 2 martin gruber anastomosis

A

fibers to FDI, AP, or FPB (thenar region)

213
Q

“all ulnar hand”

A

Riche-Cannieu anastomosis
clue: low or absent median motor CMAP but NORMAL thenar muscle strength and bulk
all ulnar hand may account for lack of thenar atrophy in CTS, but may cause thenar atrophy in ulnar neuropathy

214
Q

accessory peroneal nerve

A

terminal branch of the superficial peroneal nerve innervates EDB
occurs in approx 20% of subjects
proximal > distal amplitude

215
Q

pitfalls of repetitive stimulation

A

stimulator movement- - stable over nerve
submaximal stimulation - will not produce AP in all NMJs
recording electrode movement- changes waveform morphology
temperature - cooler temperature improves neuromuscular transmission (false negative)

216
Q

UE practical

A

median motor - APB, 7cm
median F wave - at wrist site
ulnar motor - ADM, 6.5cm, 5cm above/below
ulnar anti - ring electrodes on finger, 11cm at wrist, above elbow stim site
median ortho 2 channel - 8cm, bar electrode on elbow

217
Q

LE practical

A

fibular motor - EDB, 8.5cm and behind knee
fibular F waves
tibial motor - AH, 8cm and popliteal fossa
sural - lat malleolus, 7, 14, 21
medial plantar - bar electrode