Principle of Neuroelectrodiagnosis

Angkana Nudsasarn , MD , FRCP(T) Northern Neuroscience Center

Maharaj Nakorn Chiangmai hospital

Clinical neurophysiology

• Nerve conduction studies and electromyography• Evoked potentials• Electroencephalography• Transcranial magnetic

stimulations

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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Extracellular fl uid

Axon hillock

Saltatory conduction

Orthodromic

Antidromic

Orthodromic

Antidromic

Motor neuron

Sensory neuron

Objective of NCS

• Confirm clinical diagnosis • Localization • Pathology ( e.g. axonal vs demyelination) • Disease state • Prognosis

Common nerve• Upper extremity

–Median

– Ulnar – Radial

• Lower extremity

– Peroneal– Tibial– Sural

Nerve conduction study

What to test?• Motor –Distal latency

–Amplitude

–Velocity

• Late response - F wave

- H reflex

Nerve conduction study

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)

Kimura, Electrodiagnosis in Diseases of Nerve and Muscle: Principles and Practice

Distal stimulation

Proximal stimulation

What to measure ?

Distal latencymeasure the fastest conduction fiber

A

AB C

A BC

DE

D E

Latency abnormality

AB

C

A BC

CA

B

Amplitude We measure the sum of number of

conducted fiber

Amplitude = A+B+C+D+E

ABCDE

Amplitude abnormalityFiber A D C are sick

Only B and C can conduct

Amplitude = B plus CABC

DE

Conduction block

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

Temporal dispersion

Temporal dispersion

:The fastest conduction fiber A & B are sick because no myelin

AB

C

CA

B

Demyelination : disease of myelin

DE

Delayed DL

AB

C

A BC

CA

B

Amplitude : Not much change

Distal latency & Demyelination

DE

AB

C

A BC

CA

B

Amplitude : Not much change

Demyelination Delayed distal latency

Only fiber B & C are well

AB

C

Axonal degeneration

DE

Amplitude is small

Only fiber B & C are well

AB

C

A BC

C

Amplitude Vs Axonal degeneration

DE

Distal latency not change much

AB

C

A BC

C

Amplitude : change > 70 %

Axonal degeneration

D

Latency change < 30%

E

Axonal degeneration

Left peroneal Right peroneal

A woman with acute left foot drop

AA

BK

AK

A woman with acute left foot drop

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

Tienel’s sign was negative but Phalan’s test was positive

Right median motor

Median motor NCVsComparison of Left and Right median motor NCV

Left Right

1.56

2.5

2.5

2.4

3.9

3.8

Right median sensory NCV

!• motor amplitude is > 1 mV

F wave

H reflex

F wave

A Mallik, Conduction studies:Essential and pitfall in practice.

Ulnar nerve

Tibial nerve

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

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

Median

Left Right

Ulnar

Tibial

Left Right

Peroneal

CSF shown albuminocytologic dissociation

AIDP

H reflex

Sensory nerve conduction studyMedian orthodromic sensory study

Objective of NCS

• Confirm clinical diagnosis• Localization• Pathology ( e.g. axonal vs demyelination)• Disease state • Prognosis

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

SNAP and localization related to dorsal root ganglion

Aminoffs Electrodiagnosis in Clinical Neurology

Pattern of abnormality

Repetitive nerve stimulation test

Evaluate patients with suspected neuromuscular junction disorders

Ca2+

Ca2+

Ca2+

Action Potential

Presynaptic

Acetylcholine receptor

Postsynaptic

Normal NMJ

Ca2+

Action Potential

Acetylcholine

Acetylcholine receptor

Postsynaptic

Presynaptic

Ca2+

Action Potential

Acetylcholine

Acetylcholine receptor

Postsynaptic

Presynaptic

Immediate pool

Low rate stimulation

Low rate stimulation

The depletion of available quanta of Ach becomes more important.

< 5 HZ

Low rate stimulation

End Plate Potential

Stimulate only immediate Ach Storage

normal NMJ

Low rate stimulation

End Plate Potential

Stimulate only immediate Ach Storage

M gravis

Low rate stimulation

End Plate Potential botulism

Immediate storage depleted quickly

Katirji, B., 2007. Electromyography in Clinical Practice

Repetitive N stimulation test

Repetitive nerve stimulation test

RNS interpretation guide

• At low rate : Initial CAMP Compare 1st and 4th potential Decremental or incremetal At high rate look at the pattern

High rate stimulation

High rate stimulation

Increased of Ach Quanta release by Ca++ becomes more important

> 10 Hz

High rate stimulation

Increased of Ach Quanta release by Ca++ becomes more important

> 10 Hz

Giant CMAP

High rate stimulation

Ach quanta released by Ca++ becomes more important

> 10 Hz

normal NMJ

High rate stimulation

Ach quanta released by Ca++ becomes more important

> 10 Hz

M gravis

High rate stimulation

Ach quanta Released by Ca++ which was previously blocked by toxin becomes more important

> 10 Hz

botulism

Repetitive Nerve Stimulation

• At frequency of 30 cps !

• M.gravis shows decrementing response !

• Eaton lambert syndrome shows incremental response

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

Needle EMG

• Recording of electrical activity in muscle– Spontaneous activity – Voluntary activity – Amplitudes – Frequencies – Patterns of electrical activity – Audio and visual information

• 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

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

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

Abnormal insertional activity!!!D. Myokimic discharge!!!E. Complex repetitive discharge

Marching soldiers

Machine

A summary of characteristic findings on needle electromyography

A summary of characteristic findings on needle electromyography

A summary of characteristic findings on needle electromyography

Positive sharp wave and Fibrillation

Muscle denervation • Ant. horn cell • Root • Plexus • Nerve • Necrotizing

myopathy • Muscular

dystrophy

A man with chronic progressive generalized muscle atrophy ,fasciculation and hyperreflexia

NCS : WNL !EMG • At rest :positive sharp

wave and fibrillation +2

• MUP : small polyphasic

Dermatomyositis

Blink reflexes

Evaluation • Involvement of trigeminal or facial nerve • Variety of demyelinating polyneuropathies • Central lesion of brainstem

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)

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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PATTERN REVERSAL VEP

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

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

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

Left-sided acoustic neuroma

Aminoffs Electrodiagnpsis in clinical practice

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

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

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

Median nerve SEPs• Erb’s point :N9 brachial plexus• Cervical spine : N13 dorsal column nuclei • Scalp : N20 – P23 thalamocortical radiations &

primary sensory cortex

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)

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

Dispersed P37 potential with a prolonged latency