DR.SUBODH KUMAR MAHTO DR.SUBODH KUMAR MAHTO, PGIMER,DR.RML HOSPITAL, NEW DELHI

1. NERVE CONDUCTION
STUDIES,
ELECTROMYOGRAPH
YDR.SUBODH KUMAR MAHTO
PGIMER,DR.RML HOSPITAL,
NEW DELHI

2. CONTENTS • Approach to NCS and EMG
• Anatomy and Neurophysiology
• Fundamentals of NCS
– Basic Nerve conduction studies
– Late Responses
– Blink Reflex
– Repititive Nerve Stimulation
• Fundamentals of EMG
– Basic Overview
– Analysis of Spontaneous Activity
– Analysis of Motor Unit Action Potentials (MUAP)
• Clinical- ElectrophysiologicCorrelations

3. Approach • Serve as an extension of the clinical examination.
• Directed neurologic examination essential before EDX
studies to identify clinical abnormalities and establish a
DD.
• Individualized, based on DD & modified in real time as
the study progresses & further information gained.

4. • Used to diagnose disorders of the peripheral nervous
system
– primary motor neurons (anterior horn cells),
– sensory neurons (dorsal root ganglia),
– nerve roots,
– brachial and lumbosacral plexuses,
– peripheral nerves,
– neuromuscular junctions, and
– muscles.
• Provide diagnostic information when disorder arises in
CNS (e.g., tremor/ upper motor neuron weakness).

5. Localization is
the aim of EDx
study
The Primary motor neuron resides within
the spinal cord, whereas the primary sensory
neuron, the dorsal root ganglion, lies
outside the spinal cord.The dorsal root
ganglion is a bipolar cell. lts proximal process
forms the sensory nerve root; the distal
process becomes the peripheral sensory
nerve.

6. Disorders
of PNS

7. Nerve conduction studies
often provide further
valuable information
about the fiber types
involved and the
underlying nerve
pathophysiology and
narrow the differential
diagnosis

8. Possible
localizations
determined from
the
electrodiagnostic
study.

9. Cardinal
rules of NCS
and EMG

10. ANATOMY AND
NEUROPHYSIOLOGY

11. ANATOMY

12. • The peripheral nervous system includes
• the peripheral motor and sensory neurons; their
• primary neurons, the anterior horn cells, and dorsal root ganglia;
• the neuromuscular junctions; and
• muscle.
• The DRG, a bipolar cell located distal to the sensory root, is anatomically different
from the anterior horn cell.
• Consequently, lesions of the nerve roots result in abnormalities of MNCs but spare
the SNCs, as the dorsal root ganglion and its peripheral nervee remain intact.

13. • The motor root( from AHCs), leaves ventrally
• Sensory root enters the dorsal side.
• Distal to the DRG, the motor and sensory roots together-
form spinal nerve.
• Each spinal nerve divides- a dorsal and ventral ramus.
• Each ramus contains both motor and sensory fibers.
• The dorsal rami supply sensation to skin over back.
• The ventral rami
• continue as intercostal nerves in the thoracic region.
• In the lower cervical region, the ventral rami fuse to
form the brachial plexus.
• In the mid lumbar through sacral segments, intermix
to form the lumbosacral plexus.

15. Myotomal and peripheral
nerve innervation
Dermatomes

16. individual
peripheral nerve
anatomy
Myelinated fibers- small dark rings
(myelin) with a central clearing (axon).
The endoneurium is present between
axons.
Axons grouped into fascicles,
surrounded by perineurium (arrow).
Surrounding the entire nerve-
epineurium (large arrow).

17. PHYSIOLOGY

18. RMP and
Action
potential

19. Motor unit
• The motor unit- one axon, its anterior horn cell & all connected muscle fibers and
NMJs.
• A nerve fiber AP always results in depolarization of muscle fibers of motor unit
creating an electrical potential known as the motor unit action potential (MUAP).
• Analysis of motor unit action potentials- needle EMG examination.

20. PERIPHERAL NERVE
CLASSIFICATION
SCHEME

21. Important
points to
ponder
• Routine motor & sensory conduction velocity
& latency measurements from the largest &
fastest fibers.
• Small myelinated (Adelta, B) & unmyelinated
C -not recorded with standard NCSs-
neuropathies that preferentially affect only
small fibers may not reveal any abnormalities.
• Largest & fastest fibers , muscle afferents,
Alpha fibers (aka Ia fibers)-originate from
muscle spindles & mediate afferent arc of
muscle stretch reflex- not recorded in either
MNCs & SNCs.

22. RECORDING

23. • Process of intracellular electrical potential being transmitted through
extracellular fluid and tissue.
• volume-conducted potentials
• near-field
• far-field potentials.
• Near-field potentials can be recorded only close to their source, depend
on distance between recording electrodes & electrical source (AP).
CMAPs, SNAPs, and MUAPs, recorded during routine motor
conduction, sensory conduction, and needle EMG studies- examples.
Volume Conduction

24. Volume
conduction
and
waveform
morphology

25. NEAR FIELD
AND FAR
FIELD
POTENTIALS

26. BASIC NERVE
CONDUCTION
STUDIES
• Motor conduction studies
• Sensory conduction studies
• Mixed conduction studies
• Basic patterns

27. Motor
conduction
studies
• Performed first
• Responses in range of mV (sensory &mixed- microV)
• Less affected by technical factors
• Gain set at 2-5mV
• Recording elecrodes- belly tendon montage
– G1 (active)- centre of muscle belly
– G2 (reference)- over tendon
• Stimulus over supplying nerve with cathode closest to
electrode.
– Characteristics- duration-200 microS, current 20-50mA.
– Supramaximal stimulus essential (starting from baseline)
– Gradually increased till max potential recorded.
– Further 20% increase to ensure supramaximal stim.
• Recorded potential- CMAP (biphasic)

28. CMAP
Latency
• Time from stimulus to initial deflection from baseline
• Represents-
– Time from stimulus site to NMJ
– Time delay across NMJ
– Depolarisation across muscle
Amplitude
• From baseline to neg peak/ 1st neg to 1st pos peak
• Reflects no of muscle fibres that depolarise
• Decreased amplitude
– Loss of axons
– Conduction block
– NMJ disorders
– Myopathies
Duration
• From deflection from baseline to 1st baseline crossing
• Measure of synchrony
• Increased with slowing of some fibres but not others

29. Conduction
velocity
• DL represents:
– the nerve conduction time from the distal stimulation site
to the NMJ (A),
– NMJ transmission time (B)
– muscle depolarization time (C).
• PL represents
– distal nerve conduction time (A),
– the NMJ time (B)
– muscle depolarization time (C)
– nerve conduction time between the proximal and distal
stimulation sites (D).
• DL subtracted from PL =nerve conduction time between
the distal and proximal stim sites (D)
• conduction velocity=(distance/time).
• CV reflects only fastest fibers

30. Sensory
conduction
studies
• Only nerve fibres assessed (no NMJ, no muscle)
• Response very small (1-50microV)
• Gain set 10-20 microV
• Recording eletrodes (G1 and G2) n line 3-4 cm apart
• Stiumulus characteristcs
– Duration 100/200 microS
– Current- 5-30 mA to supramaximal stimulus(less
threshold than motor)
• Recorded potential- SNAP (biphasic/triphasic)
• CV measured from 1 stim site

31. SNAP
Latency- Onset & Peak
• Onset – time from stim to initial neg deflect (biphasic), to
the positive peak (triphasic). Represents time from stim
site to electrodes for fastest conducting fibres
• Peak- measured at the mid point of 1t neg peak. Easier to
measure
Amplitude
• From baseline to neg peak.
• Reflects sum of all individual sensory fibres that depolarise
• Low values- def disorder of peripheral nv
Duration
Conduction velocity
• From onset to 1st baseline crossing
• Typically shorter than CMAP (1.5 ms vs 5-6 ms)

32. CMAP VS
SNAP
diff in terms of size &
duration.
CMAP amplitude
measured in mV, whereas
SNAPs in microvolt range
(different gains).
CMAP negative peak
duration 5 to 6 ms, whereas
SNAP’s much shorter,
typically 1 to 2 ms..

33. Orthodromic
vs antidromic
recording
Top trace:
Antidromic study, stimulating
wrist, recording index finger.
Bottom trace:
Orthodromic study, stimulating
index finger,
recording wrist

34. Advantages
&
Disadvantages
• Advantages of antidromic over orthodromic
– Amplitude of SNAP higher
– Helpful in pathological conditions.
– Less subject to noise/artifacts.
• Disadvantages
– SNAP f/b volume conducted CMAP
– Difficult to differentiate if sensory latency is
increased.

35. Lesions Proximal to
the Dorsal Root
Ganglion Result in
Normal Sensory
Nerve
Action Potentials

36. Proximal
Stimulation:
Normal Temporal
Dispersion and
Phase Cancellation

37. Explanation • SNAPs & CMAPs both compound potentials, represent
summation of individual fiber APs.
• Some fibers that conduct faster & some more slowly .
– With distal stimulation, fast and slow fiber potentials
arrive recording site at approximately same time.
– proximal stimulation, slower fibers lag behind faster fibers.
• For sensory fibers, neg phase of the slower fibers
overlaps with pos trailing phase of fastest fibers. cancel
each other, resulting in decrease in area & amplitude
• Less for motor potentials d/t their large amplitude &
smaller range of normal CVs

38. Temporal
dispersion and
phase
cancellation
Proximal sensory fiber potentials cancel
out each other
Phase cancellation not significant for
CMAPs because of their large amplitude.

39. Mixed
conduction
studies

40. • Largest & fastest fbres, Ia, spindle afferents recorded
only in mixed studies.
• Entire nerve stimulated & recorded
• CVs faster.
• Ia fibres have highest myelin content, earliest affected
in demyelinating neuropathies (entrapment).
• Settings-
– Gain set at 10-20microV
– Recording electrodes (G1 G2) placed in line at distance 3-
4 cms
– Mixed Nerve Action Potential (MNAP)- summation of all
sensory and MFAPs- biphasic/triphasic.

41. Principles of
stimulation
supramaximal
stimulation
optimal stimulator
position

42. BASIC
PATTERNS
1. Axonal
2. Demyelination
3. Myopathy
4. NMJ disorders

43. A-normal
B-Axonal
C-Demyelination
(CV slowing only)
D-Demyelnation
(with conduction
block)

44. Patterns
B: Axonal loss. amplitudes decrease;CV is normal/slightly
slowed, but not < 75% LLN & DL is normal or slightly
prolonged, but not >130%ULN. morphology doesn’tchange
between proxim and distal sites
A: Normal study. Note the normal DL <4.4 ms, amplitude
>4 mV and CV >49 m/s.
C: Demyelination- unifom, slowing often associated with
inherited conditions (e.g.,CMT polyneuropathy). CV markedly
slowed < 75% LLN) & DL markedly prolonged (>130% ULN). No
change in config between proxim and distal stimulation sites.
D: Demyelination with CB/temporal dispersion. Marked
slowing of CV and DL with change in morphology between
distal and proxim stimulation sites associated with
acquired causes of demyelination, may be seen in GBS

45. CV slowing
in Axonal
loss
fastest- 65 m/s
slowest- 35 m/s

46. Demyelination • Essentially, any motor, sensory, or mixed nerve
conduction velocity that is slower than 35 m/s in the
arms or 30 m/s in the legs signifies unequivocal
demyelination.
Dilemma- which is what?
• Might appear that reduced amplitudes always marker of
axonal loss rather than demyelination. Not true, depends
on:
• first, whether sensory or motor studies are performed,
and
• second, whether or not conduction block is present.
• Sensory amplitudes low in demyelinating lesions. Reduced
sensory amplitudes from normal temporal dispersion and
phase cancellation, exaggerated by demyelinative slowing

47. Conduction
block
• Reduced amplitudes in demyelination seen when CB is
present, as in acquired demyelination .
• If CB is present in demyelinating lesion,CMAP
amplitude depends on stimulation site & location of CB
– CB b/w normal distal stim site & recording electrodes,
both distal and proximal CMAP amplitudes low and may
simulate an axonal loss lesion
– CB b/w distal and proxim stim sites,CMAP amplitude
normal distally, below block, but decreased at proxim
stim site, above block.
– Proximal & distal stim sites distal to block,CMAP
amplitudes- normal both distally and proximally

48. Conduction Block
In acquired demyelinating
lesions, demyelination
often patchy, multifocal
process.
When nerve
stimulated proximal to the
conduction block, the
compound muscle action
potential (CMAP) drops in
ampl-itude and area and
becomes
dispersed (

49. CMAP
amplitude
and CB
location

50. Million dollar
question- CB or
Temporal
dispersion?
use criteria of mare than 50% drop
in area between proximal and distal
stimulation sites to define
electrophysiologic CB.
remember that both CB and
abnormal temporal dispersion and
phase cancellation signify acquired
demyelination.
• A marked drop in proximal CMAP area usually means
conduction block.
• In the figure, there is no conduction block between
distal and proxim stim sites. Drop in amplitude entirely
due to abnonnal temporal dispersion from
demyelinating lesion.
• To differentiate conduction block from abnormal
temporal dispersion requires drop in area >50%.

51. Two patients
with wrist
drop- who
has the
better
prognosis?
• Patient 1- conduction block- demyelination- better
prognosis
• Patient 2- significant axonal loss with some CB across
the spiral groove- prognosis guarded

52. Conduction
block and
CIDP

53. Myopathy • Sensory conduction studies- always normal
unless a/w superimposed neuropathic
condition.
• Motor conduction studies- most myopathies
primarily affect proximal muscles.
– CMAP amplitudes and distal latencies- generally
normal ( routine MNCS record distal muscles).
– Rare myopathic disorders affect distal muscles,
and in such situations CMAP amplitudes- low.
– Even in these situations, however, DL and CVs-
normal.

54. NMJ
Disorders
• Sensory conduction studies- always normal
• Motor conduction studies-
– postsynaptic- normal
– Presynaptic-CMAPs low at rest, CVs and DL
normal.
•For diagnosis- RNS/
Exercise testing.

55. LATE
RESPONSES
F response
H reflex
Axon reflex

56. F Response

57. F Response
circuitry
• nerve stimulated distally - depolarization occurs both
orthodromically & antidromically.
– Direct muscle response (M)- orthodromic.
– F response(F)- derived by antidromic travel to AHC--
backfiring of some AHCs---orthodromic travel back down
nerve past stimulation site to muscle
• Actually a smallCMAP, representing 1-5% of muscle
fibres
• Circuitry, both afferent & efferent- pure motor
• No synapse- not a true reflex.
• Sensory neuropathy- F respose normal
• Settings- gain increased to 200 microV and the sweep to
either 5 or 10 ms.
• Measurements- minimal / maximal latency, persistence,
chronodispersion.

58. Procedure

59. Contd..
• With proximal stimulation,
proximal CMAP latencies
increase as expected, but F
response latencies decrease, d/t
F response first traveling
antidromically to spinal cord.
• Each F response varies slightly
in latency, config & amplitude-
diff population of AHCs being
activated with each
stimulation.
• shortest latency-largest and
fastest motor fibers.
• Best obtained with
distal stim

60. Contd.. • F wave persistence-
– measure of no of F waves obtained per number of
stimulations.
– Normal-80% to 100% & always above 50%.
• F wave chronodispersion-
– diff betwn fastest & slowest F response.
– Normal-up to 4 ms in the UL & up to 6 ms in LL.
• Minimal F wave latency- most reliable measurement
• F responses- absent in sleeping/sedated patients-
absent responses not necessarily sign of pathology.

61. Do F waves
assess only
proximal
segment?
• Prolonged responses
– Any nerve with prolonged DL on routine
NCS
– Generalized CV slowing in polyneuropathy
– Prolonged in legs than arms
– Taller patients
• Factors affecting F wave response
– DL
– CV
– Height
NO

62. So, Can’t we
diagnose
proximal
lesions with
F?
F ESTIMATE
F estimate = (2D/CV) x 10 + 1 ms + DL
X -time from stim site to cord; distance between stim site and cord
(D) divided byCV of the nerve
Y-turnaround time at AHC= 1 ms
Z-time from stim site to the muscle= DL
Theoretical F estimate = 2X +Y + Z. X can be calculated by measuring
the
.Thus, the F estimate = (2D/CV) x 10 + 1 ms + DL

63. • Normally, F estimate > minimal F wave latency (CV is
more in prox segments)
• Therefore, if the measured minimal F response is
prolonged compared to the F estimate
• delay in proximal nerve segments out of proportion to
what can be expected for DL, CV & height.

64. USEFULNESS
OF
F RESPONSE
• Tests the entire nerve circuit.
• Greatest usefulness in early acquired
demyelinating polyradiculopathies-
combo of normal routine NCS +
prolonged F response suggesting
proximal lesion where demyelination
starts.
• NOTE- F response 1-5% of CMAP, so
unobtainable with severely reduced
CMAP( axonal loss)

65. For
Radiculopathy
& Plexopathy?
• Limited d/t following reasons
– F responses can check only nerve/nerve
root that innervating muscle being
recorded.
• In the upper extremity, distal muscles (i.eAPB,
ADM)- innervated by C8/T1 nerve roots, rarely
affected by radiculopathy, compared with
commonly affected C5, C6, C7-
• usefulness only in assessing possibleC8-Tl
radiculopathies & L5-S1 radiculopathies
– In radiculopathy predominantly affecting
sensory nerve root fibers (initial symptoms
of pain and radiating paresthesias),F
response-normal.

66. Bottomine of
F response
• If distal nerve conductions are normal,
prolonged F response may occur in
– proximal neuropathy,
– plexopathy, or
– radiculopathy, and
• the finding cannot be used to
differentiate among those possibilities.

67. H REFLEX

68. • True reflex- sensory afferent, synapse &
motor efferent segment.
• H reflex in adults can routinely be elicited only
by stimulating tibial nerve in the popliteal
fossa, recording the gastro-soleus muscle.
• The circuitry of the H reflex involves the
– Ia muscle spindles as sensory afferents and the
– a motor neurons and their axons as efferents.
• Low sub maximal stimulus with a long
duration selectively activates the Ia fibers.

70. SUBMAXIM
AXIMAL
STIM BEST
ELICITS H
REFLEX
• at low stimulation intensities, H reflex present without
direct motor (M) response.
• With increasing stimulation, H wave grows & M response
appears.
• At higher stimulation, M potential continues to grow & H
reflex diminishes, d/t collision betwn the H reflex &
antidromic motor potentials.

71. MEASUREMENTS
& APPLICATIONS
• H reflex with shortest latency measured & compared
with set of normal controls for height
• Comparison with C/L side more useful in assessing U/L
lesion; difference >1.5 ms-considered significant.
• Max amplitude H response compared with maximal
amplitude M potential to calculate H/M ratio
• USEFULNESS
– electrical correlate of S1 ankle reflex. If ankle reflex
present clinically, H reflex should always be present.
– Any lesion that might decrease ankle reflex also might
prolong the H reflex (polyneuropathy, proximal tibial and
sciatic neuropathy, lumbosacral plexopathy & lesions of
the 51 nerve root).
– H/M ratio-crude assessment of AHC excitability-
increased in UMN lesions.

72. Axon reflex-
indicator of
renervation
following
denervation

74. REPITITIVE
NERVE
STIMULATION

75. NMJ • Electrical- chemical-electrical barrier.
• Presynaptic terminal-Ach in vesicles ka quanta (each
ha 1000 molecules)
• 3 separate stores-
– Immediately available store (1000 quanta)
– Mobilization store (10000 quanta)
– Reserve store (>100000 quanta)
• Process of transmission
• AP depolarizes presynaptic junction Ca influx via
volt gated channels quanta released Ach binds
receptors on post synaptic membrane opens Na
channels, local depolarization-EPP above threshold
causes MFAP
• Normally, EPP always above threshold by a margin
(safety factor)

76. Effect of
RNS in
normal
subjects
• Slow RNS (2-3 Hz) Quanta progressively depleted
from primary store EPP amplitude falls still
above threshold d/t safety factor MFAP with each
stimulation after few seconds, mobilisation store
repletes quanta,increasing EPP with MFAP
• Rapid RNS quanta depleted takes 100 ms to
actively pump out Ca RNS leads to accumulation of
Ca wich counterbalances quanta depletion along with
mobilization store EPP increase MFAP

77. EPP
threshold>15
mV
Rapid (50 HZ) RNS presynaptic disorder- progressive increment of
EPP amplitude to above threshold and subsequent gen of MFAP

78. Exercise
Testing-
equivalent of
Rapid RNS
• Post exercise facilitation (brief period of exercise,10 s)-
effect identical to RNS
– Normal –consistent generation MFAP-CMAP
– Postsynaptic- causes EPP to increase
• EPP above threshold at baseline- no change
• EPP below threshold- causes repair.
– Presynaptic- facilitates low EPPs- usually EPP below
threshold at baseline- MFAP is generated when nitially
there was none.
• Post exercise exhaustion- (mechanism not
understood)- after 1 min of max voluntary exercise
rises initially f/b fall over several min.
• Normal- EPP falls but never below threshold.
• NMJ disorders- Prolonged exercise- greater decline-
MFAP not generated

79. 3HzRNS in MG.
• A: Decrement of CMAP amplitude at rest.
• B: Postexercise facilitation, Decrement of CMAP immediately following 10 seconds of maximal voluntary exercise
has repaired toward normal.
• C-E: Postexercise exhaustion. Decrements of CMAP 1, 2, and 3 minutes after 1 minute of maximal voluntary
exercise. Decrement becomes progressively more marked over the baseline decrement.
• F: Postexercise facilitation after a decrement. Immediately following another 10 seconds of maximal voluntary
exercise, the decrement, which has worsened as a result of postexercise exhaustion, repairs toward normal.

80. RNS in MG
• the large decrement between the first and fourth potentials.
• After the 4th potential,the decrement not as marked- forms "U
shape."
• Decrement begins to improve when the mobilization store
resupplies immediately available store.
• Requires I to 2 secs
• highly characteristic of a true NMJ disorder.

81. RNS
protocol

82. ELECTROMYOGRAPHY
Analysis of Spontaneous Activity
Analysis of Motor Unit Action Potential

83. Clinical
implications
of
spontaneous
activity
• Distribution of abnormal activity- neuroanatomic
localization.(isolated radiculopathy, denervation potentials
restricted to muscles in same myotome).
• Type of spontaneous activity- specific diagnostic information.
(Myotonic discharges- few myopathies, hyperkalemic periodic
paralysis)
• Degree or amount of spontaneous activity determine severity.
• Information about time course.(radiculopathy, several weeks pass
before fibrillation potentials seen)

84. Analysis

85. Source
generators
from
morphology

86. • A: Miniature endplate potential (monophasic negative).
• B: Muscle fiber action potential, brief spike morphology.Triggered by needle-induced depolarization of terminal nerve twig (initial
negative, diphasic).
• C: Muscle fiber action potential, brief spike morphology (initial positive, triphasic).
• D: Muscle fiber action potential, positive wave morphology (initial positive, slow negative).
• E: Multiple different muscle fiber action potentials linked together.
• F: Motor unit action potential. Note the longer duration and higher amplitude compared with MFAP shown above.

87. Insertional
activity
• With each needle movement, normal insertional activity-
brief &usually lasts </= 300 ms
• Increased insertional activityseen in both neuropathic &
myopathic disorders.

88. Waveform
morphology
and site of
depolrization
• A:Traveling depolarizing wave create a biphasic potential if begins under recording needle electrode (initial
negative peak) & then moves away from electrode (positive peak).This is known as an endplate spike.
• B: If begins at a distance from the needle. there is initial positive deflection as it moves toward needle, f/b
negative phase as it moves beneath needle, and then final positive deflection as it travels away.This is known
as a fibrillation potential.
• Endplate spikes are differentiated from fibrillation potentials by the absence of an initial positive deflection
because the depolarization begins at the endplate.

89. Spontaneous
activity-
normal
• All spontaneous activity is abnormal exception-that
occurs at NMJ- END PLATE NOISE, END PLATE SPIKES
• End plate noise (seashell sound)
• End plate spikes(cracking, sputtering)

90. Abnormal
spontaneous
activity
Fibrillation potentials
• MFAP morphology-Brief spike initial pos deflection, 1-5
ms duration, low amplitude (10-100 microV).
• Regular, rate 0.5-10 Hz, sound like "rain on the roof.“
• Typically seen in neuropathic disorders
Positive sharp waves
• signify active denervation.
• brief initial positivity f/b long negative phase.
• sound “dull pop”, amplitude variable (10-100 microV),
regular firing, with a rate 0.5-10 Hz, up to 30 Hz.
• Graded from 0 to 4+

91. Contd..
Complex repetitive discharges
• multiple spikes (each spike representing different single muscle fiber)
• perfectly repetitive nature, machine like sound
• In chronic neuropathic/myopathic disorders; arise in any setting-
denervated muscle fibers lie adjacent to other denervated muscle
fibers.
Myotonic discharges
• Myotonic discharges-seen in myotonic dystrophy, myotonia
congenita, paramyotonia congenita.
• "rewing engine" sound on EMG, due to waxing-waning.
• a single brief run may occur in any denervating disorder

92. Abnormal
spontaneous
activity-
motor unit
potentials

93. Typical
MUAP
morphology
Fasciculations (corn popping sound), doublets
Myokymic discharges (radiation induced nerve
damage)

94. Cramps and
neuromyotonic
discharges
NEUROMYOTONIC DISCHARGES
high-frequency (150-250 Hz), decrementing, repetitive
discharges of single motor Unit, "pinging" sound
CRAMPS
high-frequency discharges of motor axons, with the
electromyogram characteristically showing MUAPs with a normal
morphology firing repetitively & sometimes irregularly at high
frequencies.

95. Rest tremor
vs
myokymia
Rest tremor
Myokymic discharges (marching sound)

96. Analysis of
motor unit
action
potentials
(MUAP)
• Attributes of MUAP-
– Morphology
• Duration
• No of phases
• Amplitude
– Stablity
– Firing characteristics
• Patterns-
– normal
– Neuropathic
– myopathc

97. Morphology
(based on
mean of at
least 20
different
MUAPs in a
muscle)
• Duration-
– Best reflects no of muscle fibres within a motor unit
– 5-15 ms
– From initial deflection from baseline to return to baseline
– Duration correlates with pitch
• Long duration sound dull and thuddy, short duration crisp
and static like
• Polyphasia, serrations & satellite potentials
– Polyphasia –measure of synchrony
• Normally MUAPS-2-4 phases
• Increased polyphasia in 5-10% in any muscle-N
• Polyphasic MUAPs- high frequency clicking
• Non specific
– Serrations- changes in direction that do not cross
baseline. Same implication as polyphasia
– Satellite potentials- in early reinnervation.

98. • Amplitude varies widely. Most MUAPs have an
amplitude >100 microV & < 2 mV. measured from
peak to peak
– Increased amplitude with (1) proximity of the
needle to the motor unit (2) increased no of
muscle fibers in motor unit (3) increased diameter
of muscle fibers (4) more synchronized firing of
muscle fibers.
• Major spike- largest positive to negative
component of MUAP

99. • Stability- measure of effective NMJ transmission.
Unstable MUAPs seen in NMJ disorders/immature NMJs
(eary reinnervation).
• FIRING FREQUENCY
– Activation- ability to increase firing rate. (central process)
– Recruitment- increase in no of firing motor units. Affected in
neuropathies.
– Interference pattern
• Normal ratio of firing frequency to no of motor units firing
5:1.

100. Normal
firing
pattern
Semirhythmic pattern
Relationship of force to firing
frequency. Maximal firing rate-
30Hz

101. Interference
patterns
• A: Normal
• B: Neuropathic.
• C: Myopathic.
• In normal subjects, so many motor unit action potentials
(MUAPs) fire during maximal contraction that
differentiating individual motor unit potentials is
difficult.
• In neuropathic recruitment, a reduced number of MUAPs
fire at a high frequency, resulting in an incomplete
interference pattern (often called the picket fence
pattern).
• In myopathic recruitment, although the number of
MUAPs is normal, the interference pattern consists of
short-duration, small amplitude MUAPs.

102. Incomplete
interference
patterns
How to
assess?

103. Poor activation
or poor
recruitment? • In the trace, the same unit (identical morphology) firing
rapidly (30 Hz)
• Ratio-30:1- poor recruitment- neuropathic pattern
Patient asked to contract maximally
• In the trace, the same unit (identical morphology) firing
at 5 Hz
• Ratio-5:1- normal recruitment- but poor activation-
central disorder (uncooperative/stroke, MS)

105. • Normal MUAPs have two to four
phases.
• In chronic neuropathic lesions (after
reinnervation), no of muscle
fibers/motor unit increases- long-
duration/high-amplitude/ polyphasic
MUAPs.
• In myopathies/NMJ disorders with
block, the no of Junctional muscle
fibers in motor unit decreases-short-
duration/ small-amplitude/ polyphosic
MUAPs.

106. CLINICAL-
ELECTROPHYSIOLOGIC
CORRELATIONS
Common patterns
Clinical cases

107. Important
points
• Time course-
– Hyperacute- <3 days
– Acute-more than several days but less than 2 weeks
– Subacute- less than several months
– Chronic- months- years
• Wallerian degeneration starts in 3-5d .
• Denervation potentials in 2-6 weeks
• Reinnervation is complete in months-years

116. Clinical syndromes