Principle of ElectroDx by Dr. Angkana Nudsasarn, Chiang Mai University
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Transcript of Principle of ElectroDx by Dr. Angkana Nudsasarn, Chiang Mai University
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Principle of Neuroelectrodiagnosis
Angkana Nudsasarn , MD , FRCP(T) Northern Neuroscience Center
Maharaj Nakorn Chiangmai hospital
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Clinical neurophysiology
• Nerve conduction studies and electromyography• Evoked potentials• Electroencephalography• Transcranial magnetic
stimulations
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Resting Membrane Potential
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Myelinated axonMyelin sheath
Node of Ranvier
Extracellular fl uid
Direction of action potential propagation
Intracellular fl uid
– –+ + +
+ + ++ + + + + +
– +–
+–
+–
– – –– – –
–
–
– – –
– – –
– – –
– – –
– – –
– – –
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– – – –
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– –+ + +
+ + ++ + +
+ + +
– + + +– – –
– – –– – –
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– – –
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– – – –
+–
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Extracellular fl uid
Axon hillock
Saltatory conduction
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Orthodromic
Antidromic
Orthodromic
Antidromic
Motor neuron
Sensory neuron
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Objective of NCS
• Confirm clinical diagnosis • Localization • Pathology ( e.g. axonal vs demyelination) • Disease state • Prognosis
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Common nerve• Upper extremity
–Median
– Ulnar – Radial
• Lower extremity
– Peroneal– Tibial– Sural
Nerve conduction study
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What to test?• Motor –Distal latency
–Amplitude
–Velocity
• Late response - F wave
- H reflex
Nerve conduction study
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What to test?
• Sensory
– Distal latency
– Amplitude
– Velocity
What to test?• Autonomic function
test – Sympathetic skin
response(SSR) – The quantitative
sudomotor axon reflex test (QSART)
– Thermoregulatory sweat test(TST)
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Kimura, Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice
Distal stimulation
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Proximal stimulation
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What to measure ?
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Distal latencymeasure the fastest conduction fiber
A
AB C
A BC
DE
D E
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Latency abnormality
AB
C
A BC
CA
B
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Amplitude We measure the sum of number of
conducted fiber
Amplitude = A+B+C+D+E
ABCDE
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Amplitude abnormalityFiber A D C are sick
Only B and C can conduct
Amplitude = B plus CABC
DE
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Conduction block
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Criteria of conduction blockDefinite • >50% drop in amplitude ,
<15% prolong duration!
• >50% drop in amplitude and area!
• >20% drop in amplitude and area over a short segment
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Temporal dispersion
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Temporal dispersion
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:The fastest conduction fiber A & B are sick because no myelin
AB
C
CA
B
Demyelination : disease of myelin
DE
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Delayed DL
AB
C
A BC
CA
B
Amplitude : Not much change
Distal latency & Demyelination
DE
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AB
C
A BC
CA
B
Amplitude : Not much change
Demyelination Delayed distal latency
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Only fiber B & C are well
AB
C
Axonal degeneration
DE
Amplitude is small
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Only fiber B & C are well
AB
C
A BC
C
Amplitude Vs Axonal degeneration
DE
Distal latency not change much
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AB
C
A BC
C
Amplitude : change > 70 %
Axonal degeneration
D
Latency change < 30%
E
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Axonal degeneration
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Left peroneal Right peroneal
A woman with acute left foot drop
AA
BK
AK
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A woman with acute left foot drop
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This 50 y.o. woman has had nocturnal numbness in both hands for 2 months.
Physical examination revealed no definite weakness nor numbness in both hands
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Tienel’s sign was negative but Phalan’s test was positive
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Right median motor
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Median motor NCVsComparison of Left and Right median motor NCV
Left Right
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1.56
2.5
2.5
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2.4
3.9
3.8
Right median sensory NCV
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!• motor amplitude is > 1 mV
F wave
H reflex
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F wave
A Mallik, Conduction studies:Essential and pitfall in practice.
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Ulnar nerve
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Tibial nerve
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Usefulness of F wave
• Testing of proximal segments • Testing long lengths of nerves • A sensitive indicator of proximal
portion• Determine the site of conduction
slowing
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Case example
• A 27 years old woman !
• Acute progressive sharp soothing pain over distal limbs for 2 weeks
!• Physical examination
– Motor gr v – DTR gr 0
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Median
Left Right
Ulnar
Tibial
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Left Right
Peroneal
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CSF shown albuminocytologic dissociation
AIDP
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H reflex
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Sensory nerve conduction studyMedian orthodromic sensory study
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Objective of NCS
• Confirm clinical diagnosis• Localization• Pathology ( e.g. axonal vs demyelination)• Disease state • Prognosis
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Typical nerve conduction study abnormalities in axon loss or demyelination
Axonopathy Demyelination
!dL !amplitude !!!CB/Temporal
!Normal or slightly prolonged !Small !!!
!Prolonged !Normal (reduced if conduction block or temporal desperion) !Present
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SNAP and localization related to dorsal root ganglion
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Aminoffs Electrodiagnosis in Clinical Neurology
Pattern of abnormality
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Repetitive nerve stimulation test
Evaluate patients with suspected neuromuscular junction disorders
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Ca2+
Ca2+
Ca2+
Action Potential
Presynaptic
Acetylcholine receptor
Postsynaptic
Normal NMJ
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Ca2+
Action Potential
Acetylcholine
Acetylcholine receptor
Postsynaptic
Presynaptic
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Ca2+
Action Potential
Acetylcholine
Acetylcholine receptor
Postsynaptic
Presynaptic
Immediate pool
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Low rate stimulation
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Low rate stimulation
The depletion of available quanta of Ach becomes more important.
< 5 HZ
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Low rate stimulation
End Plate Potential
Stimulate only immediate Ach Storage
normal NMJ
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Low rate stimulation
End Plate Potential
Stimulate only immediate Ach Storage
M gravis
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Low rate stimulation
End Plate Potential botulism
Immediate storage depleted quickly
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Katirji, B., 2007. Electromyography in Clinical Practice
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Repetitive N stimulation test
Repetitive nerve stimulation test
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RNS interpretation guide
• At low rate : Initial CAMP Compare 1st and 4th potential Decremental or incremetal At high rate look at the pattern
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High rate stimulation
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High rate stimulation
Increased of Ach Quanta release by Ca++ becomes more important
> 10 Hz
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High rate stimulation
Increased of Ach Quanta release by Ca++ becomes more important
> 10 Hz
Giant CMAP
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High rate stimulation
Ach quanta released by Ca++ becomes more important
> 10 Hz
normal NMJ
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High rate stimulation
Ach quanta released by Ca++ becomes more important
> 10 Hz
M gravis
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High rate stimulation
Ach quanta Released by Ca++ which was previously blocked by toxin becomes more important
> 10 Hz
botulism
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Repetitive Nerve Stimulation
• At frequency of 30 cps !
• M.gravis shows decrementing response !
• Eaton lambert syndrome shows incremental response
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Slow RNS and Rapid RNS
Slow RNS : 3-4 Hz stimulationRapid RNS : 20-50 Hz stimulation
Decrement in CMAP amplitude and/or area at low stimulation rates indicates a drop in the safety factor (amplitude of EPP above the threshold for action potential )for transmission both pre- or post-synaptic cause
high frequency stimulation natural facilitation isenhanced by pre-synaptic Ca++ influx
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Needle EMG
• Recording of electrical activity in muscle– Spontaneous activity – Voluntary activity – Amplitudes – Frequencies – Patterns of electrical activity – Audio and visual information
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• Distinguish myopathic from neurogenic muscle weakness
• Provide supportive evidence of pathology of peripheral neuropathy( demyelination or axonal degeneration)
• Differentiate focal nerve, plexus, or radicular pathology
• Obligatory investigation in motor neuron disease
Needle EMG
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Normal Insertional and Spontaneous Activity
• End-plate noise (solid arrows) :seashell held to the ear
!• End-plate spikes
(dashed arrow) : sputtering fat in a frying pan
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Abnormal insertional activity
A. Fibrillation potential!!
B. Positive sharp wave!!
C. Myotonic discharge
Dull pops, Rain on tin roof, tick-tock of clock
Rain on tin roof, tick-tock of clock
Drive bomber
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Abnormal insertional activity!!!D. Myokimic discharge!!!E. Complex repetitive discharge
Marching soldiers
Machine
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A summary of characteristic findings on needle electromyography
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A summary of characteristic findings on needle electromyography
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A summary of characteristic findings on needle electromyography
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Positive sharp wave and Fibrillation
Muscle denervation • Ant. horn cell • Root • Plexus • Nerve • Necrotizing
myopathy • Muscular
dystrophy
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A man with chronic progressive generalized muscle atrophy ,fasciculation and hyperreflexia
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NCS : WNL !EMG • At rest :positive sharp
wave and fibrillation +2
• MUP : small polyphasic
Dermatomyositis
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Blink reflexes
Evaluation • Involvement of trigeminal or facial nerve • Variety of demyelinating polyneuropathies • Central lesion of brainstem
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Sensory evoked potential• Demonstrate abnormal sensory
system conduction when the history and/or neurological examination is equivocal
• Reveal subclinical involvement of a sensory system
• Help define the anatomic distribution and give some insight into pathophysiology of a disease
• Monitor changes in a patient’s neurological status
visual evoked potentials (VEPs)
short latency somatosensory evoked potentials(SSEPs)
brainstem auditory evoked potentials (BSAEPs)
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Visual evoked potentials (VEPs)
• VEP wave form are extracted from the EEG by signal averaging!
• Any abnormality that affects the visual pathways or visual cortex in the brain can affect the VEP!
• Investigation of demyelinating disease, optic neuritis, and other optic neuropathies
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104
PATTERN REVERSAL VEP
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Patient with right optic neuritis, illustrating delay of the P100 component from the right eye
Left eye
Right eye
A man with history of demyelinating injury of his left optic radiation
Aminoffs Electrodiagnpsis in clinical practice
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Brainstem Auditory Evoked Potentials (BAEPs)
A test of auditory brainstem function in response to auditory stimuli (click)
It’s a set of positive wave recorded during the first 10 seconds after a click
stimuli
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Clinical useful?
• For assess conduction through lower brainstem auditory pathway
• In patient with– Multiple sclerosis – Structural lesion of brainstem – Intraoperative monitoring of auditory pathway
during neuroSx of posterior fossa tumour– Prognosis of anoxic coma in ICU
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Left-sided acoustic neuroma
Aminoffs Electrodiagnpsis in clinical practice
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Karger, Basel, 1980 .Clinical Uses of Cerebral, Brainstem and Spinal Somatosensory Evoked Potentials.
Comatose--------Recover
35-year-old woman who was comatose following a mixed drug overdose and a respiratory arrest
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Legatt AD, Arezzo JC, Vaughan HG, Jr: The anatomic and physiologic bases of brain stem auditory evoked potentials.
Loss of waves V and VI due to
brainstem infarction
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Somatosensory evoked potentials(SEPs)
• Evoked potentials of large diameter sensory nerves in the PNS and CNS!
• Used to diagnose nerve damage or degeneration in the spinal cord!
• Can distinguish central Vs peripheral nerve lesion!
• Confirmation of a nonorganic cause of sensory loss
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Median nerve SEPs• Erb’s point :N9 brachial plexus• Cervical spine : N13 dorsal column nuclei • Scalp : N20 – P23 thalamocortical radiations &
primary sensory cortex
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The lesion of proximal segment of the peripheral nerve or the cervical cord(. A prolonged N9 to N13 inter-wave peak latency beyond the upper limit of normal)
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Tibial nerve SEPs • L3 – negative peak with latency 19 ms (L3 S)nerve roots of
cauda equina • T12 - negative peak with latency 21 ms (T12 S) dorsal fibers
of spinal cord • Scalp: positive peak – P37 negative peak – N45 thalamocortical activity
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Dispersed P37 potential with a prolonged latency