1. EMG

2. Fib and pws
What correct about these signals
1. generated in the axon
2. generated in individual muscle fibers
3. usually appear with irregular firing rhythm
4. always sign of axonal pathology
5. PSW more significant in the EDX interpretation

3. Fib and pws
What is correct about these signals
1. they are generated in the axon
2. generated in individual muscle fibers
3. usually appear with irregular firing rhythm
4. always sign of axonal pathology
5. PSW more significant in the EDX interpretation

4. EDX in demyelinating neuropathy with
conduction block
Which alternative is expected EDX finding in these conditions
1. Reduced MUP amplitudes
2. Reduced CMAP amplitudes
3. Reduced fullness of interference pattern at strong contractions
4. Abundant fibs in distal muscles

5. EDX in demyelinating neuropathy with
conduction block
Which alternative is expected EDX in these conditions
1. Reduced MUP amplitudes
2. Reduced CMAP amplitudes
3. Reduced fullness of interference pattern at strong contractions
4. Abundant fibs in distal muscles

6. 56What do you call this phenomenon?

7. 56What do you call this phenomenon?
This is CRD, complex
repetitive discharges,
not myotonia
Abrupt start and stop.
No waxing and waning

8. Mechanism
CRD (M gluteus) Abrupt start and stop,
complex. No jitter between components
1
2
3
4

9. 58EMG: acute weakness
Patients with acute weakness since 2 days.
If this is GBS, which combination of findings do we get
1. normal CMAP and CV – normal MUPs and firing
2. normal CMAP , reduced CV – early reinnervation
3. Reduced CMAP ampl - first signs of denervation
4. normal CMAP, normal CV in arms and legs, reduced # F waves,
presence of A waves and abnormal interference pattern

10. 58EMG: acute weakness
CMAP and CV changes and denervation signs have not yes developed.
Weakness is due to conduction block; thus reduced F persistence and reduced EMG pattern at effort
Patients with acute weakness since 2 days.
If this is GBS, which combination of findings do we get
1. normal CMAP and CV – normal MUPs and firing
2. normal CMAP , reduced CV – early reinnervation
3. Reduced CMAP ampl - first signs of denervation
4. normal CMAP, normal CV in arms and legs, reduced # F waves,
presence of A waves and abnormal interference pattern

11. Acute weakness
History:
Formerly healthy man with acute weakness from 7 days ago,
progressive symptoms.
the patient reports double vision and an unsteady gait.
Clinical:
external ophthalmoplegia, ataxia and areflexia weak facial muscles, ptosis and reduced
mobility of the tongue general mild muscle weakness. Sensory diffusely affectedF
EDX findings con´t and QUESTION

12. Acute weakness, EDX and Questions
Question Likely diagnosis?
GBS
Lyme disease
brainstem involvement
Miller Fischer
MG
Neurography, MCS
 general slightly decreased MCV
 F latencies extended
 DLAT extended
 distal amplitude reduced, ssk In the facial muscles
 Neurography SCS
 abnormal response with low amplitudes, more than
reduced CVEMG
 reduced interference pattern, 0 fib
 autonomous tests slightly abnormal
 abnormal Blink reflex
 prolonged latency to R1 and R2

13. Acute weakness, EDX and Questions
Neurography, MCS
 general slightly decreased MCV
 F latencies extended
 DLAT extended
 distal amplitude reduced, ssk In the facial muscles
 Neurography SCS
 abnormal response with low amplitudes, more than
reduced CVEMG
 reduced interference pattern, 0 fib
 autonomous tests slightly abnormal
 abnormal Blink reflex
 prolonged latency to R1 and R2
Question Likely diagnosis?
GBS
Lyme disease
brainstem involvement
Miller Fischer
MG

14. Discrepancies
1. Good CMAP in weak muscle, no twitch at nerve stimulation.
Normal F response.
Explanation?
conduction block
recent axonotmesis
tendon rupture
pnp
MG
myopathy
2.Good finger SNAP but no sensation at stimulation
Why?
pnp
conduction block
myelopathy
the wrong digital nerve is stimulated
GBS
3. Clear sensory experience with digital nerve stimulation but
no SNAP from the wrist
Explanation?
proximal conduction block
wrong recording position
cold hand
bipolar stim pulse has been used
the stimulus too short
4. Normal MUP and low MCV
What?
axonal pnp
conduction block
demyelination
LEM
posttraumatic reinnervation

15. Discrepancies
2.Good finger SNAP but no sensation at stimulation
Why?
pnp
conduction block
myelopathy
the wrong digital nerve is stimulated
GBS
3. Clear sensory experience with digital nerve stimulation but
no SNAP from the wrist
Explanation?
proximal conduction block
wrong recording position
cold hand
bipolar stim pulse has been used
the stimulus too short
4. Normal MUP and low MCV
What?
axonal pnp
conduction block
demyelination
LEM
posttraumatic reinnervation
1. Good CMAP in weak muscle, no twitch at nerve stimulation.
Normal F response.
Explanation?
conduction block
recent axonotmesis
tendon rupture
pnp
MG
myopathy

16. 54EMG: Myasthenia?
Patient with ptosis but no arm or leg weakness. RNS in nasalis and deltoid normal.
SFEMG in orb oculi shows jitter and some blocking. Jitter abnormal in Ext dig.
1. Ocular MG
2. Generalized MG
3. Myopathy
4. Miller Fisher syndrome

17. 54EMG: Myasthenia?
Patient with ptosis but no arm or leg weakness. RNS in nasalis and deltoid normal.
SFEMG in orb oculi shows jitter and some blocking. Jitter abnormal in Ext dig.
1. Ocular MG
2. Generalized MG
3. Myopathy
4. Miller Fisher syndrome
MG classification is conventionally on clinical grounds.
Jitter is abnormal in ED in 60% of cases with Ocular MG

18. 57EMG: Myasthenia?
Patient with bilat ptosis but no arm or leg weakness. RNS in nasalis and deltoid normal.
SFEMG in orb oculi and frontalis normal.
1. Ocular MG
2. Generalized MG
3. Myopathy
4. Bell palsy

19. 57EMG: Myasthenia?
Patient with bilat ptosis but no arm or leg weakness. RNS in nasalis and deltoid normal.
SFEMG in orb oculi and frontalis normal.
1. Ocular MG
2. Generalized MG
3. Myopathy
4. Bell palsy
Normal SFEMG findings are strong indications that symptoms are NOT MG. In this case, it may be
a myopathy, often with very little of jitter abnormalities

20. 59Methods of choice
Which is the EDX method of choice for the following diagnostic questions
MG RNS
SFEMG
CTS EMG of APB and ADM
antidromic sensory neurography
GBS EMG
neurography
thermotest
Root EMG
neurography
evoked potentials
ALS EMG
neurography
Motor unit counting

21. 59Methods of choice
Which is the EDX method of choice for the following diagnostic questions
MG RNS
SFEMG
CTS EMG of APB and ADM
antidromic sensory neurography
GBS EMG
neurography
thermotest
Root EMG
neurography
evoked potentials
ALS EMG
neurography
Motor unit counting

22. In routine EMG we usually ask the patient to perform a moderate to strong
contraction, and the EMG pattern is analyzed. What should the test be called?
Give a few words of argument why each of these descriptions are less than
optimal
Interference pattern usually means 50,60Hz
Summation pattern not much summation, equally much subtraction
Pattern at strong contraction neutral but complicated term
Recruitment pattern leads thoughts to the way MU are orderly recruited

23. In routine EMG we usually ask the patient to perform a moderate to strong
contraction, and the EMG pattern is analyzed. What should the test be called?
Give a few words of argument why each of these descriptions are less than
optimal
Interference pattern usually means 50,60Hz
Summation pattern not much summation, equally much subtraction
Pattern at strong contraction neutral but complicated term
Recruitment pattern leads thoughts to the way MU are orderly recruited

24. Can a MUP have a longer total
duration than the interval
between discharges of this MUP

25. Can a MUP have a longer total duration than
the interval between discharges of this MUP
Yes. e.g. in Duchenne MD or in
early reinnervation the duration
may be > 50 msec, corresponding
to firing rate of 20Hz. With 21Hz
firing rate, the MUP “starts
before it has ended”

26. Is it possible to decide whether a recorded
EMG signal originates in the nerve or in the
muscle?
From muscle = single fibre action potentials
From nerve = MUPs

27. Is it possible to decide whether a recorded
EMG signal originates in the nerve or in the
muscle?
From muscle = single fiber action potentials
From nerve = MUPs

28. Is there any difference in MUP parameters if
the recording is obtained 1 cm or 2 cm from
the end-plate?
More dispersion away from the end-plate
(duration, complexity) [6]
2 cm 5 cm
MUP from the same MU
(simulation)

29. Is there any difference in MUP parameters if the
recording is obtained 1 cm or 2 cm from the end-plate?
Fiber velocity 4 mm/msec. Normally the time from
start to main spike is 5 msec. Thus, in this example,
4.5 (5-0.5), 2.5 (5-2.5) and 1 (5-4) msec will be
truncated, changing shape of early phase.
2 mm
20 mm
MUP from the same MU
(simulation)
10 mm

30. Is there any difference in MUP parameters if
the recording is obtained 2 cm or 5 cm from
the end-plate?
More dispersion away from the end-plate
(duration, complexity) [6]
2 cm 5 cm
MUP from the same MU
(simulation)

31. Is there any difference in MUP parameters if
the recording is obtained 2 cm or 5 cm from
the end-plate?
More dispersion away from the end-plate
(duration, complexity) [6]
2 cm 5 cm
MUP from the same MU
(simulation)

32. We sometimes record double discharges (extra discharges, ED) in
voluntary EMG. Do we require that the two discharges are identical in
shape, to separate them from occasional occurrence of discharges from
2 different MUPs
Due to rel refractory period the second
discharge is lower in amplitude (interval
dependent). The succeeding ordinary
discharge may be missing [8]

33. We sometimes record double discharges (extra discharges, ED) in
voluntary EMG. Do we require that the two discharges are identical in
shape, to separate them from occasional occurrence of discharges from
2 different MUPs
Due to rel refractory period the second
discharge is lower in amplitude (interval
dependent). The succeeding ordinary
discharge may be missing

34. See more
explanation next
slide
Initial ED due to lack of Renshaw inhibition
inhibit
Renshaw
inhibit
Renshaw
Stålberg, unpublished
initiation of act ongoing act
100 ms
In voluntary EMG Extra discharges (ED) are often seen (normal) at initiation of activity after a
short pause. Where are they generated, muscle, axon, motor neurone?
They are generated in the motor neuron, probably representing impulses that initially escape the
inhibiting effect of Renshaw inhibition, catch property (1).
Stålberg 1966
Stålberg, unpublished

35. See more
explanation next
slide
Initial ED due to lack of Renshaw inhibition
inhibit
Renshaw
inhibit
Renshaw
Stålberg, unpublished
initiation of act ongoing act
100 ms
In voluntary EMG Extra discharges (ED) are often seen (normal) at initiation of activity after a
short pause. Where are they generated, muscle, axon, motor neurone?
They are generated in the motor neuron, probably representing impulses that initially escape the
inhibiting effect of Renshaw inhibition, catch property .
Stålberg 1966
Stålberg, unpublished

36. Initial ED due to lack of Renshaw inhibition
inbit
Renshaw
inbit
Renshaw
Stålberg, unpublished
At initiation of activity, the motor neurone produces a high
firing rate (100HZ) (inferred by Stålberg). Via retrograde Renshaw
inhibition, the firing rate of the neurone is reduced and kept there.
This has been called “catch” property (Burke, Rudomin et al. 1970)
During ongoing activation, there is a balance between neurone
firings and the Renshaw inhibition. Theoretically ED may occur if
Renshaw inhibition is lacking (neuropathy?, cyanid???)
initiation steady activation

37. Critical illness: are fibrillations in these
patients usually a sign of neuropathy
(CIP)
No, seen both in CIM and CIP.
A sign of membrane hyperexcitability,
not necessarily indicating denervation

38. Critical illness: are fibrillations in these
patients usually a sign of neuropathy
(CIP)
No, seen both in CIM and CIP.
A sign of membrane hyperexcitability,
not necessarily indicating denervation

39. Critical illness: is the myosin content
lower in CIM than in CIP
Yes

40. Critical illness: is the myosin content
lower in CIM than in CIP
Yes

41. Critical illness: is sural amplitude
different in CIM and CIP
In principle normal in myopathy, but
abnormal in CIP

42. Critical illness: is sural amplitude
different in CIM and CIP
In principle normal in myopathy, but
abnormal in CIP

43. Monopolar recording. Is there any difference in the pattern at
voluntary contraction if the distance between the two recording
monopolar electrodes (“active” and “reference”) is 1 cm or 10
cm?
With 1 cm or smaller the electrodes record
to some extent from the same MUPs, and
common activity (green) is cancelled.
With separate electrodes, you will get the
difference of independent activity from the two.

44. Monopolar recording. Is there any difference in the pattern at
voluntary contraction if the distance between the two recording
monopolar electrodes (“active” and “reference”) is 1 cm or 10
cm?
With 1 cm or smaller the electrodes record
to some extent from the same MUPs, and
common activity (green) is cancelled.
With separate electrodes, you will get the
difference of independent activity from the two,
in effect a summation of acitivties.

45. The derivation is between the needle electrode (E1) and the reference (E2).
Activity from the reference is crucial:
In monopolar EMG the reference may be a surface electrode. If this is adjacent to the muscle under study,
the surface EMG signal will be seen on the baseline of the recording
In CNE the reference is the needle cannula. Activity from surrounding fibers contribute with similar signal
to the tip electrode and the ref and is therefore cancelled
Monopolar EMG. Why is the baseline
sometimes more “unstable” than with CNE

46. The derivation is between the needle electrode (E1) and the reference (E2).
Activity from the reference is crucial:
In monopolar EMG the reference may be a surface electrode.
If this is adjacent to the muscle under study, the surface EMG signal
will be seen on the baseline of the recording
In CNE the reference is the needle cannula. Activity from surrounding fibers
contribute with similar signal to the tip electrode and the ref and is therefore cancelled
Monopolar EMG. Why is the baseline
sometimes more “unstable” than with CNE

47. Can you detect the “size principle” with
conventional needle electrodes?
No, the uptake are of mono/con
electrodes is about 2 mm and the
MUP often 5-10 mm in diameter,
so you do not know if you are
recording from a small or large MU. [2]

48. Can you detect the “size principle” with
conventional needle electrodes?
No, the uptake are of mono/con
electrodes is about 2 mm and the
MUP often 5-10 mm in diameter,
so you do not know if you are
recording from a small or large MU. [2]

49. Concentric electrode has an oval recording surface: are
the MUP parameters different for transversal or
longitudinal insertion of the electrode (in relation to the
fiber direction).
Yes, but this is never taken into account. Ref values are
obtained with any electrode rotation

50. Concentric electrode has an oval recording surface: are
the MUP parameters different for transversal or
longitudinal insertion of the electrode (in relation to the
fiber direction).
Yes, but this is never taken into account. Ref values are
obtained with any electrode rotation

51. Which is the concentric needle electrode recording
uptake field (180 or 360 degree) for the duration
parameter in a MUP
Which is the concentric needle electrode recording
uptake field (180 or 360 degree) for the spiky part of
the MUP
For Duration: about 2 mm, spherical. For Spiky part,
about 0,5 mm, hemispherical[4, 5]

52. Which is the concentric needle electrode recording
uptake field (180 or 360 degree) for the duration
parameter in a MUP
Which is the concentric needle electrode recording
uptake field (180 or 360 degree) for the spiky part of
the MUP
For Duration: about 2 mm, spherical. For Spiky part,
about 0,5 mm, hemispherical[4, 5]

53. Is it possible to make sure that you are stimulating
muscle fibers directly and not intramuscular nerves in
so called direct muscle stimulation (critical illness
tests)
Yes, by measuring the jitter. < 5usec if direct
stimulation [7]

54. Is it possible to make sure that you are stimulating
muscle fibers directly and not intramuscular nerves in
so called direct muscle stimulation (critical illness
tests)
Yes, by measuring the jitter. < 5usec if direct
stimulation [7]

55. In monopolar EMG recording you often see a small
positive going signal on the end slope of the signal.
What is this, and why do you not see that in concentric
needle EMG
This is a far field signal generated at the tendon. Since it is a far field
potential it is recorded equally well with the tip as with the cannula in
the concentric electrode and therefore cancelled. [4]

56. With increasing force, the needle EMG amplitude
(envelope amplitude) increases. Why?
It is not the “size principle”, but a statistical
phenomenon, with increasing chance of recording
from the closest muscle fibers, with increasing force
level.

57. With increasing force, the needle EMG amplitude
(envelope amplitude) increases. Why?
It is not the “size principle”, but a statistical
phenomenon with increasing chance of recording from
the closest muscle fibers, with increasing force level.

58. In concentric needle electrode recordings, one can
sometimes obtain low amplitude MUP that looks “upside
down”. Explanation?
1. Signals are mainly recorded by the cannula
2. Obtained close to the tendon

59. In concentric needle electrode recordings, one can
sometimes obtain low amplitude MUP that looks “upside
down”. Explanation?
1. Signals are mainly recorded by the cannula
2. Obtained close to the tendon

60. Reinnervation. In the early stage of collateral
reinnervation (20 days) after a partial nerve lesion, you
start to see MUPs with some jittering spikes. In general
is the MUP “small” or “normal – slightly increased”?
Collateral reinnervation takes place from a normal MU, so the
reinnervated MU should be larger than a normal MU. We get small
MUs, “nascent” MUPs only after complete nerve lesion followed by
nerve regrowth.

61. Reinnervation. In the early stage of collateral
reinnervation (20 days) after a partial nerve lesion, you
start to see MUPs with some jittering spikes. In general
is the MUP “small” or “normal – slightly increased”?
Collateral reinnervation takes place from a normal MU, so the
reinnervated MU should be larger than a normal MU.
We get small MUs, “nascent” MUPs only after complete nerve lesion
followed by nerve regrowth.

62. One month of increasing muscular weakness
Background
21 yo man with slowly increasing symptoms since 1 month.
Mainly muscle pain, weakness, especially in the arms. No diurnal variation.
No trauma or other known trigger.
Since previously asthma. On one occasion venous thrombosis in the left arm.
Clinic:
cranial nerves OK with the exception of neck flexor weakness.
Arms and legs show muscular weakness proximally. Normal reflexes, Babinski plantar.
Normal sensibility in arms and legs. Normal finger-nose test. Can't walk normally
No skin abnormalities
Lab: P-myoglobin=693 (24-77)
P-Creatine Kinase=6050 (50-400)

63. Median nerve:
Q6
Neurografi

64. Ulnar nerve
Q6

65. m. Vastus lateralis dxt
Q6

66. m. Deltoideus dxt
Q6

67. m. Deltoideus dxt

68. m. Biceps brachii dxt

69. m. Biceps brachii dxt
Q6

70. Ultrasonography:
In the right Deltoid muscle there is
partiel hyperecchogenic changes
with an impression of increased
interstitel vascularisation
(as compared to m. EDC, m. Vastus
lateralis and m. Tibialis anterior).
Q6

71. Summary:
Clinical proximal weakness
Neurography normal.
EMG myopathic MUPs, IP and fibs
Ultrasound: hyperechogenicity and increased vascularization in the deltoid.
Muscle biopsy: fiber diameter variation, no grouping but other findings
Question Likely diagnosis
myositis
MND in early stages
virus
Simvastatin side effect
metabolic disorder

72. Summary:
Clinical proximal weakness
Neurography normal.
EMG myopathic MUPs, IP and fibs
Ultrasound: hyperechogenicity and increased vascularization in the deltoid.
Muscle biopsy: fiber diameter variation, no grouping but other findings
Question Likely diagnosis
myositis
MND in early stages
virus
Simvastatin side effect
metabolic disorder

73. Q5
30 year old woman
Past history: depression, ME/CFS, back problems
Currently:
A week with acute pain in the right and after a few days also the
left shoulder/upper arm. Some pain in right leg. Weakness in
painful areas.
Rheumatologist assesses pat has reactive arthritis - gives
steroids.
Then neurologist consultant. Finds the diagnosis unclear and
suggests neurophysiology

74. Q5
Neurological examination
Right-sided scapulae alata
Bilateral weakness: Finger extension, wrist extension (and flexion).
reduced sensibility over the right thumb and radially on the forearm
Neurography:
Motor MCV and F-responses: N. medianus and nervus ulnaris: Normal MCV and Normal F-laten
Sensory SCS: Right n. cutaneous antebrachii lateralis: Low amplitude
Normal findings forN. medianus (Volar, finger 1 and 3),
n ulnaris ( finger 5),n. radialis, n. cutaneus antebrachii medialis

75. Q: Most likely diagnosis:
a. Parsonage Turner syndrome
b. MND
c. radiculopathy
d. focal accessory damage
e. “flail arm”
Q5
EMG:
Right m. biceps brachii, m. deltoideus bilat, left m. flexor carpi radialis and m. flexor carpi ulnaris. - NORMAL
Right m. serratus anterior: Normal amplitude and duration of MUPs. Fibrillation potentials and positive sharp
waves ++.
Bilat m. flexor pollicis longus: 0 MUPs. Fibrillation potentials and positive sharp waves ++
Right m. extensor digitorum: Slight MUP changes Fibrillation potentials and positive sharp waves +.

76. Reference List
1. Burke RE, Rudomin P, Zajac FEIII. Catch property in single mammalian motor units. Science.
1970;168:122-4.
2. Ertas M, Stalberg E, Falck B. Can the size principle be detected in conventional EMG recordings?
Muscle Nerve. 1995;18:435-9.
3. Gydikov A, Kosarov D. Extraterritorial potential field of impulses from separate motor units in
human muscles. Electromyography Clinical Neurophysiology. 1972;12:283-305.
4. Nandedkar SD, Sanders DB. Recording characteristics of monopolar EMG electrodes. Muscle
Nerve. 1991;14:108-12.
5. Nandedkar SD, Sanders DB, Stålberg E. Selectivity of electromyographic recording techniques; a
simulation study. Med Biol Eng Comput. 1985;23:536-40.
6. Stålberg E, Karlsson L. Simulation of the normal concentric needle electromyogram by using a
muscle model. ClinNeurophysiol. 2001;112:464-71.
7. Stålberg E, Trontelj JV, Mihelin M. Electrical microstimulation with single-fiber
electromyography: a useful method to study the physiology of the motor unit. Journal of
Clinical Neurophysiology. 1992;9:105-19.
8. Stålberg E, Trontelj JV, Sanders DB. Single Fiber EMG. 3rd ed. Uppsala: Edshagen Publishing
House; 2010.