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1 of 21
EMG, routine
Fib and pws
Factors 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
Fib and pws
Factors 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
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. Interference pattern at strong contraction most pronounced proximally
5. Abundant fibs in distal muscles
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. Interference pattern at strong contraction most pronounced proximally
5. Abundant fibs in distal muscles
56What do you call this phenomenon?
56What do you call this phenomenon?
This is CRD, complex
repetitive discharges,
not myotonia
Abrupt start and stop.
No waxing and waning
Mechanism
CRD (M gluteus) Abrupt start and stop,
complex. No jitter between components
1
2
3
4
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, recured # F waves, presence of A waves
- abnormal interference pattern
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, recured # F waves, presence of A waves
- reduced interference pattern
Acute weakness
History:
Formerly healthy man with acute weakness from 7 days ago,
progressive symptoms.
the patient reports double vision and an unsteady gait.
Clinic:
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
Acute weakness, EDX and Questions
Question Likely diagnosis?
GBS
Lyme disease
brainstem involvement
Miller Fischer
MG
Question What is your next step
RNS
outpatient CFS analysis
test for antibodies against cholinergic receptor
SFEMG
admission for diagnosis and treatment
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
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
Question What is your next step
RNS
outpatient CFS analysis
test for antibodies against cholinergic receptor
SFEMG
admission for diagnosis and treatment
Discrepancies
70. Good CMAP in weak muscle, no twitch at nerve
stimulation.
Normal F response.
Explanation?
conduction block
recent axonotmesis
tendon rupture
pnp
MG
myopathy
71.Good finger SNAP but no sensation at stimulation
Why?
pnp
conduction block
myelopathy
the wrong digital nerve is stimulated
GBS
72. 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
73. Normal MUP and low MCV
What?
axonal pnp
conduction block
demyelination
LEM
posttraumatic reinnervation
Discrepancies
71.Good finger SNAP but no sensation at stimulation
Why?
pnp
conduction block
myelopathy
the wrong digital nerve is stimulated
GBS
72. 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
73. Normal MUP and low MCV
What?
axonal pnp
conduction block
demyelination
LEM
posttraumatic reinnervation
70. Good CMAP in weak muscle, no twitch at nerve
stimulation.
Normal F response.
Explanation?
conduction block
recent axonotmesis
tendon rupture
pnp
MG
myopathy
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
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
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
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
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
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

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EMG routine

  • 2. Fib and pws Factors 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 Factors 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. Interference pattern at strong contraction most pronounced proximally 5. 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. Interference pattern at strong contraction most pronounced proximally 5. 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, recured # F waves, presence of A waves - 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, recured # F waves, presence of A waves - reduced 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. Clinic: 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 Question What is your next step RNS outpatient CFS analysis test for antibodies against cholinergic receptor SFEMG admission for diagnosis and treatment 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 Question What is your next step RNS outpatient CFS analysis test for antibodies against cholinergic receptor SFEMG admission for diagnosis and treatment
  • 14. Discrepancies 70. Good CMAP in weak muscle, no twitch at nerve stimulation. Normal F response. Explanation? conduction block recent axonotmesis tendon rupture pnp MG myopathy 71.Good finger SNAP but no sensation at stimulation Why? pnp conduction block myelopathy the wrong digital nerve is stimulated GBS 72. 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 73. Normal MUP and low MCV What? axonal pnp conduction block demyelination LEM posttraumatic reinnervation
  • 15. Discrepancies 71.Good finger SNAP but no sensation at stimulation Why? pnp conduction block myelopathy the wrong digital nerve is stimulated GBS 72. 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 73. Normal MUP and low MCV What? axonal pnp conduction block demyelination LEM posttraumatic reinnervation 70. 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