CNP Course - NCS Flashcards
Median Motor muscle
APB
Median motor G1 site
APB 1/3 from wrist
Median motor distal stim site
wrist, b/w FCR and palmaris longus
median motor proximal stim site
elbow, over brachial pulse
median motor distance from G1
7cm
ulnar motor muscle
ADM
ulnar motor G1 site
1/2 from origin
ulnar motor distal stim site
volar wrist, radial to FCU
ulnar motor proximal stim site
5cm distal to medial epicondyle
5cm proximal to medial epicondyle
ulnar motor distance from G1
6.5cm
peroneal motor muscle
EDB
peroneal motor G1 site
mid EDB muscle
peroneal motor distal stim site
ant ankle lat to TA
peroneal motor proximal stim site
behind knee
peroneal motor distance from G1
8.5cm
tibial motor muscle
AH
tibial motor G1 site
1cm below/behind navicular
tibial motor distal stim site
1-2cm behind/above medial malleolus
tibial motor proximal stim site
popliteal fossa
tibial motor distance from G1
8cm
blink motor muscle
orb oculi
blink motor G1 site
on line with pupil
blink motor G2 site
lateral palpebral fissure
blink motor stim site
supraorbital notch
blink motor distance from G1
no standard distance
facial motor muscle
nasalis
facial motor G1 site
1cm above nares
facial motor G2 site
same on opposite side
facial motor stim site
below lobe, ant/low mastoid
facial motor distance from G1
no standard distance
median anti G1 site
ring D2 proximal phalanx
median anti G2 site
3.5-4cm distal to G1
median anti distal stim site
b/w FCR and PL volar wrist
median anti proximal stim site
elbow over brachial pulse
median anti distance
13cm
ulnar anti G1 placement
ring D5 proximal phalanx
ulnar anti G2 site
3.5-4cm distal to G1
ulnar anti distal stim site
volar wrist, radial to FCU
ulnar anti proximal stim site
5cm proximal to medial epicondyle
ulnar anti distance
11cm
median ortho/palmar G1 site
distal: wrist
proximal: block over nerve at elbow
median ortho/palmar G2 site
3.5-4cm distal to G1
median ortho/palmar stim site
thenar crease 2nd MC
median ortho/palmar distance
8cm
ulnar ortho/palmar G1 site
distal: wrist
proximal: block over nerve at elbow, 5cm proximal to medial epicondyle
ulnar ortho/palmar G2 site
3.5-4cm distal to G1
ulnar ortho/palmar stim site
hypothenar crease 4th MC
ulnar ortho/palmar distance
8cm
radial sensory G1 site
on nerve over EPL
radial sensory G2 site
4cm distal to G1 on 2nd MC/FDI
radial sensory distal stim site
2/3 forearm, dorsal radius
radial sensory proximal stim site
elbow b/w lat biceps hooked under brachioradialis
radial sensory distance
10cm
superficial peroneal sensory G1 site
3cm proximal to 1/2 line between lateral malleolus and AT tendon
superficial peroneal sensory G2 site
3.5-4cm distal to G1
superficial peroneal sensory stim site
anterolateral fibula
superficial peroneal sensory distance
14cm
sural G1 site
behind lateral malleolus
sural G2 site
3.5-4cm distal to G1, below lateral malleolus
sural stim site
point A, B, C, all post 1-3cm lateral to midline
sural distance
A- 7cm, B- 14cm, C- 21cm
medial plantar G1 site
block 1cm proximal to medial malleolus over artery
medial plantar stim site
med plantar fascia, 2cm distal to navicular tubercle
medial plantar distance
12-14cm
lateral plantar distance
block 1cm proximal to medial malleolus over artery
lateral plantar stim site
2.5-3cm lateral to stim site of medial plantar
lateral plantar distance
14-16cm
why perform motor NCS
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”)
cathode does what
negatively charged and depolarizes the axon
anode does what
positively charged and hyperpolarizes axon
reversal of cathode-anode can cause
inaccurate distance measurement (error of 3cm may be made)
anode block
prolonged distal latency
difficulty in nerve localization situations
unfamiliar with anatomy
limb edema
post-trauma or surgery
large body habitus
common sites: elbow, radial nerve, Erb’s point
effect from difficulty in nerve localization
submaximal stimulation
higher stimulus intensity -> current spread to other nerves, increased discomfort
what is the technique used to optimally localize the nerve being tested?
sliding
understimulation (submaximal stimulation)
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
minimize understimulation by
observe waveform
increase intensity: 10% > maximal
reduce impedence
increase cathode-anode separation
acceptable reduction in amplitude and area between distal and proximal sites
<20% reduction in amplitude and area
if waveforms dissimilar, think of
understimulation
overstimulation
stimulation of adjacent nerves at one site and not the other
anomalous connections between nerves
temporal dispersion
common uses of arm motor NCS
upper extremity mononeuropathy (CTS, ulnar neuropathy)
arm pain (cervical radiculopathy)
brachial plexopathy
peripheral neuropathy
myopathy
NMJ disorder
motor neuron disease
short segment incremental stimulation
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
focal nerve compression - neuropraxia
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
situations of neuropraxia
cool
ischemia
local anesthetic
compression
NCS errors
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
inaccurate measurement of nerve length correction
tape measure follow course of nerve
wrong distal distance correction
accurately measure before and after stimulation
initial positive CMAP deflection correction
move G1 electrode
ensure not overstimulation or stimulator near ulnar nerve
different form or size of the CMAP at the two sites of stimulation correction
check for submaximal stimulation at elbow
failure to localize nerve correction
sliding
cool limb temperature correction
monitor continuously and warm limb
musculocutaneous uses
musculocutaneous mononeuropathy
upper trunk plexopathy
multifocal motor neuropathy
peripheral neuropathy (absent distal responses)
NMJ disorders (repetitive stimulation)
radial EDC uses
radial neuropathy
wrist drop
posterior cord plexopathy
multifocal motor neuropathy
radial motor muscle
EDC
radial motor G1 site
middle of EDC on dorsum of forearm
radial motor distal stim site
bw biceps tendon and brachioradialis
radial motor proximal stim site
lateral border of triceps at deltoid insertion
radial motor distance
10cm distal to lateral epicondyle
musculocutaneous motor G1 site
1/2 distance between tendons of origin and insertion of biceps over center of muscle belly
musculocutaneous distal stim site
under biceps tendon
musculocutaneous proximal stim site
Erb’s point
axillary motor uses
axillary mononeuropathy
upper trunk, posterior cord plexopathy
NMJ disorder (repetitive stimulation)
axillary G1 site
1/2 distance b/w acromium and along a line which bisects the deltoid, insertion of the deltoid
axillary distal stim site
Erb’s point
suprascapular uses
suprascapular neuropathy
upper trunk plexopathy
suprascapular G1 site
2cm below scapular spine, midway b/w medial border of scapula and acromium
utility of sensory NCS
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
SNAPs
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
SNAP amplitude
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”
SNAP conduction velocity
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
shock artifact reduced by
skin prep - abrade and clean
ground
minimize paste
minimal intensity and duration
slide
orientation - ‘rotate’
averaging sensory NCS
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
correct motor artifact
ensure electrodes away from metacarpal-phalangeal joint
wrap gauze around ring electrodes
temperature effects on NCS
cool temp:
- increases amplitude
- slows CV
- prolongs distal latency
onset latency
used when measuring conduction velocity in SNAPs
peak latency
used when measuring distal latency in SNAPs
recording errors in sensory NCS
inadequate skin prep
wrong location
plugged in wrong
electrodes not plugged into the preamplifier
median sensory NCS uses
carpal tunnel syndrome
median mononeuropathy
polyneuropathy
cervical radiculopathy (should be normal)
brachial plexopathy
ulnar sensory uses
ulnar neuropathy
polyneuropathy
polyradiculopathy
cervical radiculopathy (should be normal)
brachial plexopathy
radial sensory uses
radial neuropathy
cervical radiculopathy (should be normal)
brachial plexopathy (upper trunk, posterior cord)
polyneuropathy (esp when superimposed possible CTS and ulnar neuropathy)
polyradiculopathy
lateral antebrachial cutaneous uses
musculocutaneous neuropathy
brachial plexopathy (upper trunk, lateral cord)
medial antebrachial cutaneous uses
brachial plexopathy (lower trunk, medial cord)
C8-T1 radiculopathy (should be normal)
ulnar neuropathy (should be normal)
pitfalls of sensory NCS
technically more difficult than motors
more prone to artifact, noise
very low amplitudes
why perform leg NCS
leg pain (radiculopathy)
peripheral neuropathy (length-dependent)
lower extremity mononeuropathy (e.g. fibular)
polyradiculopathy
NMJ disorders
myopathy
motor neuron disease
limitations of LE NCS
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)
fibular motor uses
peripheral neuropathy
lumbosacral radiculopathy (L5)
lumbosacral plexopathy
sciatic neuropathy
fibular mononeuropathy
motor neuron disease
NMJ disorder (EDB rarely helpful)
myopathy (rarely helpful)
if amplitude at knee is larger than ankle for fibular motor
check for understimulation at the ankle
check for overstimulation at the knee
stimulus behind the lateral malleolus (accessory fibular nerve)
fibular f-waves…
often absent, even on normal patients
superficial fibular sensory uses
peripheral neuropathy
lumbosacral radiculopathy (L5) - usually normal, may be abnormal
lumbosacral plexopathy
sciatic neuropathy
fibular mononeuropathy
superficial fibular sensory G1 site
3cm proximal to midpoint bimalleolar line, between lateral malleolus and AT tendon
superficial fibular sensory stim site
over superficial fibular nerve on lateral calf just anterior to fibula
superficial fibular sensory distance
14cm
tibial motor uses
peripheral neuropathy
polyradiculoneuropathy
lumbosacral radiculopathy (S1)
lumbosacral plexopathy
sciatic neuropathy
tibial mononeuropathy
motor neuron disease
tibial motor accepted amplitude reduction
up to 50% amplitude reduction from ankle to knee
medial and lateral plantar sensory uses
peripheral neuropathy
polyradiculoneuropathy
lumbosacral radiculopathy
lumbosacral plexopathy
sciatic neuropathy
tibial mononeuropathy
tibial H reflex uses
S1 radiculopathy
Lumbosacral plexopathy
sciatic neuropathy
what is H reflex
stimulate Ia afferent fibers (sensory)
- action potential propagates orthodromically
- at cord, few AHCs depolarize
- action potential down motor axons
electrophysiologic correlate of “achilles” reflex
how to perform H reflex
selectively stimulate sensory fibers by:
- low stimulus intensity
- higher stimulus duration
H reflex errors
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
sural sensory uses
peripheral neuropathy
polyradiculoneuropathy
lumbosacral radiculopathy (normal)
lumbosacral plexopathy
sciatic neuropathy
tibial mononeuropathy
femoral motor uses
upper lumbar radiculopathy (normal)
lumbosacral plexopathy
femoral neuropathy
NMJ disorder (e.g. LEMS)
femoral motor G1 site
over the center of the rectus femoris, 1/2 way between the inguinal ligament and patella
femoral motor stim
monopolar surface prong
single prong held in the femoral triangle, just lateral to femoral pulse, may have to be pushed deep into the tissue
saphenous sensory uses
upper lumbar radiculopathy (normal)
lumbosacral plexopathy
femoral neuropathy
why assess proximal nerves or roots?
proximal mononeuropathies
radiculopathies
polyradiculopathy
brachial plexopathy
cranial neuropathies
NMJ disorders
techniques available to assess proximal nerves
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
F waves
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
F-waves morphology
vary in latency and morphology
Jendrassik maneuver may enhance activation
percentage varies with the nerve (least with peroneal)
F wave errors
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
axon reflex - A wave
motor stimulation - action potential propagates antidromically toward AHC, but loops through a collateral sprout and returns orthodromically to muscle
H wave vs. F wave
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
form of direct proximal nerve stimulation
Erb’s point
Erb’s point
supraclavicular fossa: 1/2 distance from acromium to sternum
requires pressure
rotate to direct current spread
criteria for abnormality at Erb’s point stimulation
low amplitude or no response
amplitude reduction from upper arm site
- ulnar/hypothenar >20% (or >10m/s slowing of CV)
- musculocutaneous/biceps >20%
pitfalls of erb’s point
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)
why perform repetitive stim
suspect NMJ disorder (MG, LEMS)
nonspecific weakness’
exclude myasthenia gravis in patient with fatigue, dysarthria, diplopia
pre-synaptic vs post-synaptic
children
NMJ physiology
- action potential
- Ca2+ channels open
- synaptic vesicles released
- ACh binds receptor
- sodium channels open
- sodium influx
- generation of end plate potential
- muscle fiber contraction
factors that determine MEPP (and EPP) size
number of ACh molecules per quanta
structure of synapse
number and function of AChR
number and function of AChE
repetitive stimulation does what to safety factor
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
effect of stimulation frequency at slow rates (2-5Hz)
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
effect of stimulation frequency at fast rates (10-50Hz)
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)
normal RNS
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
disorders of neuromuscular transmission if EPP is marginally above threshold
slow rates result in lower amplitude EPP
EPP may not reach threshold
neuromuscular transmission may fail
decrease in the number of muscle fibers contracting
disorders of neuromuscular transmission if EPP is just below threshold
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
poor RNS technique can result in
false negative study
false positive study
excess pain
excess time of the study
frustration
RNS technique
limb immobilization
supramaximal stimulation with as small a stimulus as possible
Distal nerves tested in RNS
ulnar and peroneal
(median, anconeus)
proximal nerves tested in RNS
spinal accessory
(axillary, musculocutaneous, femoral)
cranial nerves tested in RNS
facial
(trigeminal)
brief exercise findings and when to perform
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
brief exercise path
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
when to perform 1 minute exercise
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
criteria of abnormality on RNS
conservative criteria of abnormality: decrement of at least 10% in 2 different muscle/nerve preparations
- tapering pattern
- repair after exercise
- post exercise exhaustion
TRUE decrement
baseline testing: reproducible degree
baseline: stable
largest drop: between 1st and 2nd stimulus
pattern of decrement: tapering
following brief exercise: repair
FALSE decrement
baseline testing: variable decrement
baseline: noisy or variable
largest drop: variable (“roller coaster”)
pattern of decrement: variable
following brief exercise: no repair
diseases with decrement
neuromuscular junction
- myasthenia gravis, lambert eaton, drugs/toxins
nerve terminal disorders
- progressive MND (e.g. ALS), early reinnervation, polyradiculopathy (GBS)
falsely negative RNS
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
technical errors in RNS suspected if
results are not reproducible
pattern or envelope of decrement, increment, post exercise potentiation or exhaustion are unusual
baseline shifts
changes in configuration
protocol for generalized MG - high suspicion
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
protocol for generalized MG: low suspicion
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
when to perform 10sec exercise
want to assess for facilitation
- abnormal decrement or low amplitude CMAP (? LEMS)
- isometric for 10seconds
- normal or MG should improve decrement slightly
when to perform 1min exercise
want to assess for exhaustion (worsening decrement)
- isometric exercise for 1 minute
- stimulate at 30, 60, 120, 180, and 240 seconds after exercise
presynaptic NMJ disorders
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
blink reflex
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)
prolonged latency of R1 and bilateral R2s when stimulating involved side
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
stimulate affected side, prolonged or absent R1 and R2, contra R2 is normal
facial nerve lesion
stimulate normal side, ipsi R1 and ipsi R2 are normal, contra R2 prolonged
blink reflexes in peripheral neuropathies
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
utility of facial NCS
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
potential pitfalls to facial NCS
high stimulus intensity required to maximally stimulate facial nerve
volume conduction from overstimulation and masseter response
facial NCS prognostic parameters in Bell’s palsy
latency
amplitude
threshold excitability
latency in facial NCS prognostication of Bell’s Palsy
5-7 days.
longer latency (0.6ms longer) with reduced amplitude may develop associated synkinesis
amplitude in facial NCS prognostication of Bells palsy
<10% of unaffected side, poorer recovery (>6 months, synkinesis)
10-30% recovery between 2-8 months
>30% good prognosis within 3 months
threshold excitability in facial NCS prognostication of Bells palsyy
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
differential diagnosis of abnormal facial movements
blepharospasm
tics
focal motor seizure
hemifacial spasm
myokymia
synkinesis (from bell’s palsy)
hemifacial spasm NCS
lateral spread
hemifacial spasm EMG
bursts (10-200msec) of single or few MUP
variable interval between bursts (20-225ms)
high firing rate within burst (200-300Hz)
synkinesis
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
needle EMG in cranial muscles
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
types of pitfalls in NCS
technique-related
physiologic
anomalous anatomy
interpretation
identifying technical errors
pay close attention to details of technique
close scrutiny of waveforms
don’t only look at numerical data
imprecise nerve localization situations
unfamiliar with anatomy
limb edema
post-trauma or surgery
large body habitus
common sites: sural, tibial (knee), radial, Erb’s
effect of imprecise nerve localiz\ation
submaximal stimulation
higher stimulus intensity
- current spread to other nerves
- increased discomfort
understimulation
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
effect of stimulator pole separation
narrow: fewer nerves stimulated, more localized site of stimulation, lower amplitude
wider (monopolar stimulator): more nerves stimulated, more current spread, more spread along nerve
overstimulation effects
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)
methods to correct overstimulation
small, incremental increase in stimulus intensity (e.g. 5-10mA)
sliding technique
observe muscle contraction
observe waveform morphology for change
clues to inappropriate G1 placement motor studies
positive initial deflection (all stim sites)
unexpectedly low amplitude
atypical waveform morphology
cool temperature pathophysiology
ion channels remain open longer -> prolonged action potential, prolonged depolarization of the excitable nerve membrane, prolonged repolarization
cool temperature NCS effect
slowed conduction velocity
prolonged distal latencies
higher amplitude responses
improves neuromuscular transmission
motor artifact
may be misinterpreted as sensory response
can interfere with precise measurement on sensory
most commonly seen in antidromic studies
correct motor artifact
placement of ring electrodes
assess peak latency with G1 movement
martin gruber anastomosis
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
type 1 martin gruber anastomosis
ulnar NCS: elbow CMAP >20% lower than wrist, below elbow CMAP similar to AE
median APB: normal results
type 2 martin gruber anastomosis
fibers to FDI, AP, or FPB (thenar region)
“all ulnar hand”
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
accessory peroneal nerve
terminal branch of the superficial peroneal nerve innervates EDB
occurs in approx 20% of subjects
proximal > distal amplitude
pitfalls of repetitive stimulation
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)
UE practical
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
LE practical
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
