Neurophysiological examinations for Vth year medical students

Neurophysiological
examinations
Edina Timea Varga MD
University of Szeged, Department of Neurology
Vth year
13th September 2019.

Themes
22. NCS and EMG in neurology practice. (ENS, EMG: examination,
indication, interpretation of results, repetitive nerve stimulation:
examination, indication, interpretation of results)
9. EEG and evoked potentials in neurology practice. (Physiological
basis of EEG, types of waves, indications, physiological basis of VEP,
AEP, SSEP indications)

Neurophysiological examinations
Central nervous system :
EEG - electroencephalography
Somatosensory evoked potential
(SSEP)
Visual evoked potential (VEP)
Brainstem acustic evoked potential
(BAEP)
Motor/magnetic evoked potential =transcranial
magnetic stimulation (MEP/TMS)
Examinations of autonomic nervous system
Sleep medicine
Peripheral nervous system:
Nerve conduction study
(NCS)(electroneuropgraphy – ENG)
Repetitive nerve stimulation
(RNS)
Electromyography (EMG)

I. Theoretical basis of neurophysiological examinations
II. NCS – nerve conduction study
III. RNS – repetitive nerve stimulation
IV. EMG – electromyography
V. EEG – electroencephalography
VI. Evoked potentials
VII. Case reports
VIII.Summary

http://outreach.mcb.harvard.edu/animations/actionpotential_short.swf
axonmembrane

Resting potential
-70 uV
axonmembrane

axonmembrane
Na+/K+ pump: 3 Na+ out, while K+ in

axonmembrane
Na+/K+ pump: 3 Na+ out, while K+ in
depolarisation

axonmembrane depolarisation

repolarisation
axonmembrane

axonmembrane return to resting potential

Purves et al. Life The Science of Biology IVth Edition 1995.
pair of electrodes
Representation of action
potential on oscilloscpe/screen
Oscilloscope/screen
membránpotenciál(mV)
 Pair of electrodes detect action potential (AP) on
the membrane surface of axons, while voltage is
changing
 Alternating electric charges on two plates makes
electron beam sweep across screen
 Oscilloscope amplifies the signals
 Amplified signal from axon moves electron
beam up and down.
 When inside of axon is positive, beam moves
up, when inside of axon is negative, beam
moves down.
Action potentials travel
along axons

Types of conduction
http://biology4isc.weebly.com/peripheral-ns.html
myelinated axon
(wrapping of Schwann cell
membranes)
pure axon
Node of
Ranvier
Myelin
sheeth
Propagating AP
Depolarisation
propagates
saltatory conduction(fast)
propagation of AP point
by point
(slow)
AP – action potential

research daily routine
diagnostics treatment

axon
node of Ranvier
myelin sheath
myelin sheath
1 mm
Nucleus of
Schwann cell
NCS – nerve conduction study
Peripheral nerves:
 sensory
 motor
 mixed
myelinated (thick, fast)non-myelinated (thin, slow)
type of
fiber
role diameter (m) conduction velocity
(m/s)
A proprioception, somatomotor 12-20 100
A touch, pressure 5-12 30-70
A motor (muscle spindle) 3-6 15-30
A pain (cold, touch) 2-5 12-30
B pregangionar autonomic <3 3-15
C temperature, mechanoceptor 0.4-1.2 0.5-2
postganglionar autonomic 0.3-1.3 0.7-2.3

• Informed consent of patient
• Adequate question on referral
• No contraindication
• skin infection
• implanted electric device <10 cm distance
• Patient in a laying comfortable position
• Cleaning, preparing the skin
• Ground electrode
• Registering electrodes
• aktive
• reference
• Skin temperature / heating in case of need
(lower limb>30 C, upper limb>32 C)
• Direct current stimulationregistration of compound AP
• Data analyses

Every peripheral nerve can be investigated (+some cranials, e.g. facial nerve)!!!

amplitude
amplitude
Amplitude:
 number of fibers
 fiber density
 skin temperature latency
∆T
Conduction velocity:
fiber diameter
myelin sheath
skin temperature
DL – distal latency (=onset latency)
CV – conduction velocity voltage
time
CV=distance/T

CV=distance/T
amplitude : axonal loss
DL  or  CV: demyelination
∆T
In case of severe axonal loss, conduction velocity,
because the fastest fibers are first lost.

Indication of nerve conduction
studies

tunnel syndromes (=compression neuropathies) (e.g. carpal,
ulnar, peroneal tunnel sy,…)
mononeuropathy (e.g. facial palsy, radial palsy, axillary nerve lesion,
pyriformis sy…)
polyneuropathy (e.g. diabetic, paraneoplastic, herediter…)
plexus lesion (e.g. brachial, lumbosacralis plexopathy…)
radiculopathy (e.g. low back pain  LV-SI…)
diff.dg.: NCS as a part of complex neurophys.study (e.g. motor
neuron disorders…)
Peripheral demyelinating neuropathies:
Guillain-Barré syndorme (GBS), chronic inflammatory
demyelinating polyneuropathy (CIDP), multifocal motor
neuropathy (MMN) …..
Every peripheral nerve can be investigated (+some cranials, e.g.
facial nerve)!!!
NCS is frequently a part of a more complex examination when
other studies are also performed (like EMG, TMS…)

Median nerve motor conduction
left right
Normal values*:
Amplitude: 6 mV
Distal latency: 4.0 ms
Conduction velocity: 50 m/s
*Normal values according to: gender, age, height; skin temperature >32 C°
Amplitude: 5.1-5.0 mV
Distal latency : 4.0 ms
Conduction velocity: 52.9 m/s
Amplitude: 0,54-0.54 mV
Distal latency : 4.6 ms
Conduction velocity : 44.3 m/s
50 Year female,
CSS, mononeuritis
multiplex
 amplitude = axonal loss
 latency,  CV = myelin loss
Interpretation of NCS results

Normal values * :
Amplitude: 15 uV
Conduction velocity: 50 m/s
Amplitude: 15.3 uV
Amplitude: 1.3 uV
 amplitude = axonal loss
50 year female,
CSS, mononeuritis
multiplex
*Normal values according to: gender, age, height; skin temperature >32 C°
left right

• axonal /demyelinating injury
• focal/genearlised
• localisation
↓amplitude=axonal loss
↓conduction velocity=demyelination
↑latency=demyelination

focal demyelination (wrist)
carpal tunnel syndrome
treatment depends on severity
http://www.naturalstateclinic.com/carpal-tunnel-syndrome
https://medlineplus.gov/carpaltunnelsyndrome.htm
https://en.wikipedia.org/wiki/Carpal_tunnel_syndrome
- clinical example

Investigation of neuromuscular junction (NMJ)
http://stevegallik.org/sites/histologyolm.stevegallik.org/images/motorendplates.jpg
RNS – repetitive nerve stimulation

http://stevegallik.org/sites/histologyolm.stevegallik.org/images/motorendplates.jpg

Indication of repetitive nerve
stimulation

http://mytips10.blogspot.hu/2016/01/myasthenia-gravis-mg-
disease-signs-symptoms-diagnosis-and-treatment.html
http://www.myastheniagravis.cz/15-english/45-ocular-myasthenia
Myasthenia gravis (MG)
Lambert-Eaton Myasthenic syndrome (LEMS)
(mitochondrial myopathy)

Performing repetitive nerve stimulation
• skin infection
• implanted electric device <10 cm distance
• Cleaning, preparing the skin
• Registering electrodes
• aktive
• reference
• Skin temperature / heating in case of need
(lower limb>30 C, upper limb>32 C)
• Several runs of electric stimulation (direct current)
– one run=10 stimulations
• Start with low frequeny stimulation, than increase (3,5,10,20,30,50 Hz)
• Data analyes

• Amplitude of registered motor action potentials:
• Decrease after each other= decrementum
(>10%) – abnormal myasthenia gravis
• Increase after each other=incrementum
(>120%) – abnormal  LEMS
• Sensitivity of RNS:
• Ocular MG= 50%,
• Generalised MG= 75%
Glostrup, KNFA
Interpretation of repetitive nerve
stimulation

Performing EMG - electromyography
• skin infection
• relative contraindication: anticoagulation
• Cleaning the skin
• Insertion of registering electrode
(within the needle: active+reference)
• Data analyses

• 1. Relaxed muscle: no electric
activity.
• 2. Mild voluntary contraction:
motor action potentials (MUP):
• all fibers from the same motor unit
• MUP’s duration and amplitude depends
on number of muscle fibers
• 3. Maximal voluntary contraction
(interference pattern):
• Coactivation of MUPs: pattern density
• MUP’s amplitude: pattern amplitude
Performing EMG - electromyography

EMG I. – Relaxed muscle: is there a spontaneous activity?
If yes=abnormal. Neurogenic/myogenic.
Normal
Denervation: spontaneous
firing of motor end plate
(muscle fiber is not linked to
the motor axon)
Collateral
reinnervation→
large MUPs
Loss of motor fibers Reinnervation

Spontaneous aktivity
i m. add. magnus in a
patient with L4 disc
protrusion
Di-/triphasic waves,
positive sharp waves
EMG I. – Relaxed muscle: spontan muscle activity:
fibrillation

Fasciculation (ALS – tongue)
Bi-/triphasic
potentials
EMG I. – Relaxed muscle: spontaneous muscle activity:
fasciculation, fibrillation…

EMG I. – Relaxed muscle: spontaneous muscle activity:
myotonic discharges

 MUP: motor unit potential –
motor unit: motor fibers activated by
one motor axon
 Calculation of all MUP’s:
 amplitude
 duration
 number of phases
 Average duration: 8-12 ms
 Average amplitude : 300-1000 µV
 Normal value depends on
 MUSCLE
 AGE
normal
neurogenic
EMG II. – mild contraction : analyses of MUPs
normal values can differ in every labs!

EMG II. – mild contraction : analyses of MUPs

EMG III. – maximal voluntary contraction
Normal pattern
interference pattern

myogenic
normal
neurogenic
EMG III. – maximal voluntary contraction

• Neurogenic OR myogenic lesions?
• Organic / psychogenic origin?
• Acute / chronic? Signs of reinnervation?
• Localisation
• Frequently analysed with other data (e.g. NCS, TMS…)
• Therapeutic approach: targeted injection of botulinum toxin……
Indication of EMG

Abnormalities in case of NEUROGENIC lesion
1. At rest:
• no abnormal in case of chronic neurogeni lesion
• abnormal firing in acute lesion: either fibrillation, fasciculation….
2. Mild contraction: high amplitude, wide, polyphasic MUPs
3. At maximal voluntary contraction (interference pattern):
• reduced
• high amplitude
Interpretation of EMG

1. At rest:
• No abnormality
• Abnormal: fibrillation /myotonic dyscharges…
2. Mild contraction: small amplitude, narrow MUPs.
3. Maximal voluntary contraction (interference pattern):
• full
• low amplitude
Abnormalities in case of MYOGENIC lesion

neurogenic/myogenic lesion
acute/chronic
reinnervation
↓amplitude, ↓duration,↑polyphasy, low ampl. IF→myogenic
↑ amplitude, ↑ duration,↑ polyphasy, high ampl, reduced IF →neurogenic
prescence of abnormal resting activity
reinnervation potentials
interference pattern (IF)

EEG - electroencephalography
ion-invasive
invasive EEG/ECO-
electrocorticography
https://neurosurgerycns.wordpress.com/2011/11/21/
http://www.reggeliujsag.ro/az-epilepszia-es-tunetei/
video-EEG
EMU (epilepsy monitoring unit)
LTM (long-term monitoring)
at department/portable

EEG - electroencephalography
Alving, Sabers&Uldall: Basisbog i epilepsi
Janszky és Fogarasi: Klinikai epileptológia 2017.
http://www.reggeliujsag.ro/az-epilepszia-es-tunetei/

International 10/20 system
F – frontal
P – parietal
T – temporal
O – occipital
C – central
Fp – frontopolar
z - zero (Fz, Cz, Pz)
A – auricular
Position of EEG electrodes
Electroencephalography and Clinical Neurophysiology. 106 (3): 259–261.

Frequency bands
Delta <4Hz
Theta 4-8 Hz
Alpha 8.5-12 Hz
Beta 13-30 Hz
Gamma >30 Hz
Amplitude (adult)
10-100 uV

Theta 4,5-8 Hz
Frequency bands

Normal background activity (adult)

Amplitude reduction for eye closure

EEG provocation test I. hyperventilation
normal, 8 years old

VIDEO
EEG provocation test II. photic stimulation

REM – rapid eye movement
Sleep stage IV. REM
PSG - polysomnography

EEG is abnormal if:
1. slow background activity
2. asymmetry
3. epileptic discharges
3. abnormal amplitude
4. focal/regional/generalized alterations
5. specific patterns (e.g. for photic stimulation)
6. artefacts

Epileptiform dyscharges
• SPIKE wave
• Bispike- polyspike wave
• Spike and slow-wave
• Polyspike and slow-wave
• Sharp wave
What to document:
Localisation (one or more foci), frequency, duration, amplitude, frequency,
ictal/interictal
http://eegpedia.org

Left temporal spike and slow-wave
…and sharp waves

Left temporal delta activity and spike

Generalized spike-and-slow-wave activity
IGE – idiopathic generalized epilepsy

Myoclonus
(generalised polyspike and slow-waves)

left temporal spike and slow-wave, sharp waves
http://www.radiologyassistant.nl/en
TEMPORAL LOBE EPILEPSY

• Desorientation
• Epilepsy (diagnosis, classification, follow-up)
• Psychogenic seizures
• Focal/generalized slowing (EEG only localises but dos NOT give proper
diagnosis!)
• (brain death – in some countries it is obligatory)
Indication of EEG

• Information and informed consent of patient
• Cleaning/preparing the skin
• Placement of electrodes
• Recording during rest (laying)
• Opening/closing eyes
• Photic stimulation
• Hyperventilation
• If possible: sleeping/awakening
• Seizure detection
• Special provoking factors (unconscious patient, reflex epilepsy…)
• If needed: sleep deprivaton EEG (lasts>1,5 hours)
Performing routine EGG (30 minutes)
https://www.epilepsygroup.com/notes6-35-63/how-is-an-electroencephalogram-
eeg-used-in-epilepsy-wha.htm
https://www.brainlatam.com/products/eeg-electrode-caps

Interpretation of EEG
1. Background activity (alpha: normal)
2. Asymmetry?
3. Epileptiform discharges
3. Amplitude abnormalities
4. Focal/regional/generalised patterns (even if single slow wave)
5. Specific patterns e.g. after provocation
6. Artefacts
7. Clinical incidence

Evoked potentials
(EP)
•VEP – visual evoked potentials
•(B)AEP (=ABR, BERA) – (brainstem) auditory
evoked potential
•(S)SEP – (somato)sensory evoked potentials
• MEP – motor evoked potential /TMS – transcranial magnetic
stimulation

https://www.uspharmacist.com/article/optic-neuritis-a-brief-review
https://emedicine.medscape.com/article/1214270-overview
Handbook of Clinical Neurology Volume 102, 2011, Pages 205-221.
VEP - visual evoked potential

Clinical Neurophysiology 3rd Edition, pp:312-322.
Non-invasive, cheap, fast
Sensitive for: optic nerve / chiasma anterior lesions
Monocular stimulation
unilateral retrochiasmal lesion
bilateral optic nerve or retrochiasmal lesion

http://tidsskriftet.no/article/3011088/en_GB

Optic nerve lesion? Demyelnisation? (e.g. optic
neuritis, multiple sclerosis)
chiasma anterior lesion
unilat. retrochiasmal lesion
bilateral optic nerve or retrochiasmal lesion
Indication of VEP

Interpretation of VEP
(localises, does NOT give proper diagnosis!)
 latency
 amplitude
 interocular amplitude difference (ischaemia, compression)
 interocular latency difference (unilateral inflammation, demyelnisation)
 limited ability for localisation
NOT specific for any disorders!
Left optic neuritis

Tidsskr Nor Legeforen nr. 9, 2013; 133: 960 – 965.
Peripheral and central auditory pathways
Alert, cooperative/newborn/sedated/intellectual
disability/coma
Indication: acusticus neurinoma, multiple sclerosis,
brainstem tumor, newborn’s hearing, prognosis of
coma patient.
Sensitivity at pontoceberellar angle: 75-100% (>CT,
<MR)
Brainstem auditory evoked potential - BAEP
Performing BAEP (30-45 minutes, noninvasive):
1. detection of hearing threshold
2. electric click noise
3. monoauricular stimulation (10-11/sec), 65-70 dB over hearing threshold
4. contralateral ear is covered/hearing is masked

I. wave: N. VIII.
III. wave : cochlear nucleus,
oliva superior
IV-V. waves :
lemniscus lateralis-
colliculus inferior
IPL – interpeak latencies:
I-III, III-IV.
http://www.myvmc.com/investigations/brainstem-auditory-evoked-potential-baep/
Interpretation of BAEP

Stimulating of mixed periheral nerve/skin touch sensation information
about: (proximal) peripheral (thick, myelinated) and central somatosensory
pathways (posterior column, lemniscus medialis, spinocerebellar tract)
Investigation of proprioceptive pathways
indication: investigation of central sensory pathways
Demyelination (also subclinical stage)
Ruling out somatisation
If MRI is contraindicated
Somatosensory evoked potentials- SEP
www.accessanesthesiology.com lower amplitude, than in case of stimulating thick peripheral nerves

Tidsskr Nor Legeforen nr. 9, 2013; 133: 960 – 965.
Perofrming
somatosensory
evoked potentials- SEP
Registration sites:
 Peripheral: popliteal fossa/Erb’s point
 Central: thoracal XII, cervical VI, cranial
(ipsi- and contralateral somatosensory
cortex)

Median nerve SEP
Missing cortical waves in case of a MS patient

Tibial nerve SEP
Missing cortical waves in case of a MS patient

MEP - motor evoked potentials
(=TMS –transcranial magnetic
stimulation)
(investigation of pyramidal tract)
http://www.gettyimages.co.uk/detail/photo/woman-having-a-transcranial-magnetic-high-res-stock-photography/487737741

Contraindications of NCS, EMG, RNS, EPs
General considerations:
skin lesion
infection
(electrodes for EEG can be placed of
craniectomy place if skin is intact,
but amplitude will be high – bone
does not reduce)
Electric stimulation (ENG, RNS, SEP):
stimulator should be placed >10 cm
distance form device (PM, ICD, DBS,
VNS…)
no repetitive stimulation on that side (F-
wave, repetitive nerve stimulation)
Realtive contraindication of
needle EMG:
therapeutic anticoagulation

Case I.
• 50 year-old male, nighttime numbness for >3
months
• In the past 2 weeks: difficulties while
opening a bottle/using key
• Abnormal in neurological examination:
• paraesthesia
• abd.dig.min. and I. dorsal interosseus muscle
paresis: MRC: 4/5.
• Peripheral/central lesion?
• Which test to choose?
• NCS result:

conduction block
Ulnar nerve NCS

Ulnar nerve compression
neuropathy at elbow
conduction block
Ulnar nerve NCS

Ulnar nerve compression neuropathy at elbow=
cubital tunnel syndrome

Case II.
Difficulties
while
muscle
relaxation…

Myotonic discharges on EMG at rest
EMG

Myoclonus
(generalised polyspike and slow waves)

Purves et al. Life The Science of Biology IVth Edition 1995.
pair of electrodes
Representation of action
potential on oscilloscpe/screen
Oscilloscope/screen
membránpotenciál(mV)
 Pair of electrodes detect action potential (AP) on
the membrane surface of axons, while voltage is
changing
 Alternating electric charges on two plates makes
electron beam sewwp across screen
 Oscilloscope amplifies the signals
 Amplified signal from axon moves electron
beam up and down.
 When inside of axon is positive, beam moves
up, when inside of axon is negative, beam
moves down.
Action potentials travel
along axons

Neurophysiological examinations for Vth year medical students

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