ELECTROMYOGRAPHY

AND EVOKED
POTENTIALS
CORRY MAHAMA
DIVISI NEUROFISIOLOGI
BAGIAN/KSM NEUROLOGI
ELECTROMYOGRAPHY (EMG)
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• Performing a thorough clinical evaluation
• Conducting the needle exam:
• Preparing the pt
• Selecting appropriate muscles to test
• Inserting and moving the needle electrode
• Collecting the data
• Recognizing special situations related to the ability to examine
muscles
• Analyzing the recorded activity
• Recordings are made with a disposable concentric needle
electrode inserted into the muscle.
• A fine wire in the axis of the needle is insulated from the shaft,
the end of the needle being cut at an acute angle.
• The area of the recording surface determines the volume of
muscle that the needle can ‘‘see’’. Conventional EMG needles
record from a hemisphere of radius of about 1 mm.
• Within this volume there are some 100 muscle fibres. The many
hundreds of muscle fibres belonging to one motor unit are
distributed widely throughout the cross section of the muscle
and, therefore, within the pick-up region of the needle there may
be just 4–6 fibres of a single motor unit.
• Analysis of the waveforms and firing rates of single motor or
multiple motor units can give diagnostic information.

J Neurol Neurosurg Psychiatry 2005

Types of needle electrodes
• Monopolar needle
• Stainless steel
• Fine point insulated

• Standard or concentric needle

• Bipolar needle
• Single-fibre needle
EMG components
• Insertional activity
• Examination of muscle at rest
• Spontaneus activity
• Analyzing the motor unit
• Recruitment
Insertional activity
• If the needle is properly placed in the muscle you are
testing, you will hear and see brief electrical activity
associated with needle movement
• Healthy muscle at rest, electrically silent, as soon as
needle movement stops
• Normal  only last a few hundred miliseconds, just
barely longer than the needle movement itself
• Decreased  atrophied muscle (less muscle tissue)

• Increased  muscle pathology;* may precede actual

denervation; last > 300 msec
 Exam of the muscle at rest
• Spontaneous activity
• Abnormal
• Denervation potentials  misnomer
• Endplate region
• Where the nerve enters the muscle
• Reposition (not likely to ascertain anything; quite painful)
• 3 sign:
1. MEPP  spontaneous release of Ach @presynaptic terminal;
o short duration (1-2 msec); irreg activity every few seconds/>;
o small (10-20 mV); monophasic negative (upward) waveforms
2. Endplate spikes  single muscle fibre depolarizations;
o Biphasic, initial negative deflection
o Intermediate amplitude (100-200 mV); longer duration than MEPP (3-5 mSec)
o irregular
3. Pain
Spontaneous activity

• Fibrillation,

• Positive sharp waves,

• Complex repetitive discharges

• Fasciculation

• Myotonia

• Myokimia
Analyzing the motor unit
• Ask pt to minimally contract the muscle
• Sweep speed: 10 msec/div; gain 200-500 mV/div
• Components of the Motor Unit:
1. amplitude,
2. rise time,
3. duration
4. phases.
Recruitment
• orderly addition of motor
units so as to increase
the force of a
contraction.
• A contraction becomes
stronger in two ways:
the firing motor units
increase their rate of
firing and additional
motor units commence
firing.
Somatosensory Evoked Potentials (SSEP)
• Pre- & post- synaptic responses

• Recorded over limbs, spine, scalp following stimulation of

peripheral mixed motor & sensory nerves or cutaneus
sensory nerves.
• Analogous to standar peripheral sensory nerve
conduction studies
 But assess both peripheral & central SS conduction pathways

• Main value: provide a measurement of sensory

conduction in proximal peripheral nerves, spinal cord &
brain
• Purpose & Role:
• Assess integrity of peripheral & central SS pathways
• Identify abnormalities in the spinal cord, brainstem, or cortex
• Provide objective evidence of CNS dysfunction
• Assist in localization of sensory symptoms to proximal peripheral
nerve (roots), spinal cord or cerebral site.
GENERATORS & ORIGIN OF SEPs
• The potentials recorded during SEP represent activity in
the proprioceptive sensory system
• The responses are conducted by large diameter,
myelinated, fast-conducting fibers in the periphery and
by the dorsal column-medial lemniscus and
spinocerebellar pathways in the CNS
• Responses obtained with stimulation of cutaneus sensory
nerves or dermatomes have a lower amplitude than those
with mixed nerve stimulation.
METHODS
• Obtained with electrical stimulation of a peripheral nerve
(wrist or ankle)
• Stimulation is performed with a cutaneous stimulator,
fixed over the nerve with an elastic strap
• The stimulus intensity should produce a small twitch of
the muscle or be 2–2.5 times the sensory threshold.
• Stimulus rates of 2–5 Hz are used in the upper limb and
1–2 Hz in the lower limb.
• The highest amplitude SEPs are obtained with ulnar,
median, or tibial nerve stimulation.
• Bilateral tibial nerve stimulation may enhance the
identification of subcortical peaks.
STANDARD METHODS FOR RECORDING
• The amplitude of the SEP responses is inversely proportional
to the square of the distance between the recording
electrode and the generator of the response.
• Potentials that travel along nerve fibers or tracts are called
traveling waves, while those generated in nuclei or synapses
are called stationary waves.
• NFPs represent a propagating action potential recorded as it
passes under the recording electrodes. FFPs represent
stationary potentials generated by action potentials distant to
the recording site.
• SEP amplitudes are very low compared to other electrical
generators in the body; hence, large number of stimuli must
be averaged to obtain reproducible responses. Muscle
artifact is a major technical challenge in recording SEPs
MEDIAN AND ULNAR MIXED NERVE SEPs
• SEP waveform nomenclature is derived from the direction of
the peak deflection (P = positive or downward deflection, N =
negative or upward deflection) and the average latency of the
response.
• The major clinically important waveforms with median nerve
stimulation are N5, N9, N11, N13, N14, and N20.
• N5 represents the propagating nerve action potential from the
median or ulnar nerve at the elbow.
• N9 represents the propagating nerve action potential passing
through the brachial plexus.
• N11, N13, and N14 represent activity in the nerve root entry
zone and dorsal columns in the cervical spinal cord.
• N20 represents potentials generated over the primary
somatosensory cortex.
TIBIAL MIXED NERVE SEPs
• The major clinically important potentials with tibial nerve
stimulation are the N8, N22, N30, and P38 potentials.
• The N8 potential represents the periph- eral nerve action
potential recorded at the popliteal fossa.
• The N22 potential represents the post- synaptic potentials
generated in the dor- sal horn of the spinal cord in the
cauda equina.
• The N30 potential represents activity recorded in the
dorsal columns in the cervical spinal cord.
• The P38 potential represents activity recorded over the
primary somatosensory cortex.
 CUTANEOUS NERVE
STIMULATION SEPs
• Stimulation of cutaneous nerves:
sural, superficial peroneal, and
lateral femoral cutaneous nerves
in the lower extremity and the digital,
superficial radial, and other nerves
in the upper extremity readily elicits a
scalp SEP in normal subjects.
• However, the amplitude of the
potentials is much smaller than
those obtained with mixed nerve
stimulation, and responses are not
obtained over the spine.
• Cutaneous nerve stimulation is used
①to assess the integrity of specific
cutaneous nerves that are not readily
studied with conventional nerve
conduction study techniques,
②to evaluate isolated root function,
③to assess patchy numbness for
medicallegal reasons
DERMATOMAL SEPs
• Dermatomal stimulation is
used occasionally to assess
function of the lumbosacral
and cervical nerve roots.
• Stimulation sites are the
thumb (C6), adjacent sides of
the index and middle fingers
(C7), little finger (C8), the
dorsal surface of the foot
between the first and second
toes (L5), and the lateral side
of the foot (S1).
• Stimulation sites and normal
values are available for the
cervical, thoracic, and
lumbosacral levels.
 SEP Interpretation
• The first important step in interpreting SEP studies is close examination of the
recording to determine whether all the normally appearing components are
present.

• The absence of a main ulnar or median SEP component almost always

indicates an abnormality. Similarly, the absence of a waveform that is easily
recorded on the contralateral side also indicates an abnormality.

• Occasionally, the lumbar and cervical responses following tibial nerve

stimulation are absent in normal subjects and frequently absent in older and
obese subjects, particularly if they have difficulty relaxing. Stimulation of the
nerve is performed twice to assess for reproducibility of the recorded
responses, which helps to assess technical reliability.

• Subcortical or peripheral potentials may be low in amplitude or absent, but

because of central amplification and several parallel central pathways, a
relatively normal scalp response may still be obtained. Avoid making
statements about pathologic conditions, because disease-specific changes
are not observed with SEP studies.
Factors That Affect the Amplitude and
Latencies of the Evoked Response
• Age
• Body height dan limb length
• Temperature
• Sedative medication
• Muscle artifact
• Electric artifact
• Filter setting
Key points
• Absence of any waveform with median or ulnar nerve
stimulation is abnormal.
• Absence of lumbar or cervical potentials with tibial nerve
stimulation is commonly seen due to muscle artifact,
especially in older individuals.
• Sedation or bilateral tibial nerve stimulation may help with
detection of subcortical peaks when recording tibial SEPs.
• Body height, limb length, temperature, and other technical
factors are important in recording SEPs and may affect
interpretation of the SEP.
LOCALIZATION
• Interpeak latency determinations are desirable because
they eliminate the effects of height, limb length, and
temperature.
• Amplitude of the SEP waveforms is less useful than
latency prolongation because of the broad range of
normal values for amplitude. A 50% or greater asymmetry
in amplitude between sides may be clinically important.
• Interpeak latency prolongations imply a lesion between
the generators of the two peaks involved.
• Absence of subcortical peaks, which is more common
with tibial nerve SEPs, may point to a nonlocalized lesion
of central pathways especially if a lumbar N22 response
can be recorded.
LOCALIZATION
• Peripheral neuropathies and other periph- eral nerve
lesions typically produce pro- longed absolute latencies,
but normal interpeak latencies unless there is a sep- arate
additional lesion of the CNS.
• SEPs may be recorded from the scalp even with severe
peripheral neuropathies, a phenomenon known as central
amplifi- cation of the response.
• • SEP may help in localization of brachial plexus lesions,
but often must be inter- preted along with results of
conventional needle EMG.
• • SEP is rarely useful in routine evaluation of
radiculopathies.
• SEPs are most useful clinically in evaluation of suspected
MS, where they are highly sensitive for clinically
undetected spinal cord lesions.
• Tibial SEPs are more likely to be abnormal in MS than
median SEPs, due to the greater length of the pathways
involved from the lower extremities.
• The usual SEP abnormality in MS is prolongation of
interpeak latencies but preserved waveforms with normal
amplitudes.
• Other spinal cord lesions may produce absent or reduced
amplitude SEP responses, with variable effects on inter-
peak latencies.
• SEP latencies may be prolonged in a variety of brain stem
or supratentorial processes, including ALS,
spinocerebellar ataxias, Freidrich’s ataxia, and other
disorders.
• Giant cortical SEPs may be seen with various forms of
cortical myoclonus.
• Absence of cortical SEP responses or significant
asymmetries in coma may predict a poor prognosis for
recovery.
• Absence of cortical SEP responses may provide
confirmatory evidence for brain death.
 BRAIN STEM AUDITORY EVOKED
POTENTIALS (BAEP)
• assess the peripheral and central auditory conduction pathways.

• to assess for lesions or disorders in the CNS, and they are usually
abnormal in patients with lesions involving the auditory portion of
CN VIII, the auditory pathways in the brain stem, or both
• may be performed in awake and cooperative patients or those with
an altered mental status
• are usually performed with a click stimulus that is delivered
monaurally and that activates the peripheral and central auditory
pathways.
• Auditory stimuli cause sequential activity in CN VIII, the cochlear
nucleus, the superior olivary nucleus, the lateral lemniscus, and the
inferior colliculus.
• GENERATORS
• It is not known whether BAEPs are generated by nuclei, tracts, or a
combination of the two. The following waves are routinely measured during
BAEP testing:
• I  the distal action potential of CN VIII and appears as a negative
potential at the ipsilateral ear electrode. If wave I is absent, central
auditory conduction cannot be assessed reliably.
• II  may be generated by either the ipsilateral proximal CN VIII or the
cochlear nucleus.
• III  is likely related to activation of the
ipsilateral superior olivary nucleus.
• IV  is produced by activation of the
nucleus or axons of the lateral
lemniscus.
• V  appears to result from activation
of the inferior colliculus.
• VI and VII are presumed to be
generated by the medial geniculate
body and the thalamocortical
pathways, respectively.
Methods
• BAEPs are performed by stimulating the auditory nerve,
typically with square wave clicks and recording the
evoked response from the scalp.
• Every BAEP study should begin with an assessment of
peripheral auditory function and a bedside test of auditory
acuity should be conducted to determine the hearing
threshold.
• After assessing peripheral auditory acuity, the BAEP study
is performed.
• The time required to perform BAEPs depends on several
clinical factors, but the study usually can be completed in
30–45 minutes.
• BAEPs are evoked with electrical square wave clicks.
• Stimulus intensity should be 65–70dB above the click
hearing threshold for optimal waveform recognition.
Monaural stimulation with contralateral masking noise
provides optimal recognition of unilateral auditory pathway
lesions.
• Failure to identify wave I can be improved with techniques
such as changing stimulus intensity, changing click
polarity from rarefaction to condensation clicks, slowing
the stimulus rate, using tiptrodes, or decreasing muscle
artifact.
• The contralateral ear channel recording may help in
identification of wave II and in distinguishing wave IV from
wave V.
 FACTORS AFFECTING THE BAEP
RESPONSE
• BAEP latencies are longer in infants under the age of 2 and in
adults over 60, and are longer in men than women.
• Peripheral hearing loss may cause absence of wave I, delayed
absolute latencies of all waveforms, or distorted or absent
waveforms beyond wave I.
• Stimulus rates greater than 10Hz may increase the BAEP
latencies and decrease amplitudes.
• Stimulus intensities less than 65–70dB above hearing
threshold may increase absolute and interpeak latencies,
decrease amplitude, and alter waveform morphology.
• Changing polarity of the click may affect the amplitude and
morphology of wave I.
INTERPRETATION OF BAEPs

• Absolute and interpeak latencies (waves I–III, III–V, and I–

V) are used in the interpretation of the BAEP study.
• The most common abnormality with CNS disease is a
prolonged I–V interpeak latency.
• Determination of the region of prolongation using the I–III
and III–V interpeak latencies assists in determining
anatomical localization of the lesion.
CLINICAL APPLICATIONS

• BAEPs are useful in the diagnosis of acoustic neuromas.

The most sensitive abnormalities are an absolute or
asymmetric prolongation of the wave I–III interpeak
latency.
• The characteristic BAEP changes are prolonged I–V and
I–III interpeak latencies ipsilateral to the tumor.
• BAEPs may be abnormal when the findings of other
audiometric studies and even neuroimaging studies are
normal.
• Normal BAEP results in a patient with symptoms
suggestive of acoustic neuroma, such as dizziness and
hearing loss, argue strongly against the diagnosis.
• Abnormal BAEP results are common in patients with
clinically definite MS.
• BAEPs may be abnormal in patients with suspected MS
who do not have evidence of brain stem lesions.
• BAEP results in patients with demyelinat- ing disease
include a unilateral or bilateral prolonged I–V interpeak
latency and a decreased V/I amplitude ratio.
• BAEPsareabnormalinmostpatientswith brain stem tumors.
• Extra-axial tumors may not be associated with BAEP
abnormalities unless there is direct compression on and
disruption of the brain stem.
• BAEPs may provide prognostically important information
about outcome in comatose patients; patients with absent
BAEPs are unlikely to survive.
• The brain-dead person invariably has abnormal BAEPs,
with the characteristic findings of the bilateral absence of
all waveforms or the presence of wave I and the absence
of waves II–V bilaterally.
BAEP in peripheral Acoustic disorders

• Purpose and role

• BAEPs can be used to evaluate CN VIII and ascending brain stem
pathways.
• The test helps to differentiate cochlear from retrocochlear
pathology in patients with complaints of hearing loss, tinnitus,
dizziness, unsteadiness, or facial weakness.
• Stimuli
• Stimuli are usually brief (50–100μs) clicks that disperse acoustic
energy and provide good synchronization of neural discharges.
• Because hearing losses can affect BAEP results, pure-tone
audiometry is recommended prior to BAEP evaluation.
Interpretation
• Latencies of all BAEP waves may be delayed by both
conductive and SNHL.
• A 0.4-ms shift can be expected for each 10 dB of conductive
hearing loss.
• Age and temperature usually do not affect the interpretation of
these results.
• Sedative effects on the BAEP are minimal with the response
never being totally eliminated by anesthetics.
• Interaural latency differences are an important BAEP
measurement.
• Wave-V latency differences between ears can be influenced by
hearing loss.
• Normal variability for interaural latency differences is 0.4 ms.
• Interpretation of results is based on absolute latencies,
interaural latency differences, and interpeak intervals.
• Absolute latencies are often influenced by peripheral
(conductive, cochlear) disorders, that is, the greater the
degree of hearing loss, the greater the latency delay.
• Interaural latency differences for wave V allow for the
patient to serve as his or her own control.
• Interaural latency differences greater than 0.4 ms are
often considered suggestive of CN VIII disorders.
• Interpeak intervals are increased by lesions of CN VIII,
the pons, and medulla.
• Interpeak intervals are not affected by moderate-to-severe
levels of cochlear or conductive hearing loss.
VISUAL EVOKED POTENTIALS (VEP)
• Noninvasive studies

• measure the evoked responses to visual stimuli

• assess the visual conduction pathways through the optic

nerve and brain.
• Allow quantitative determination of visual function

• Highly sensitive to lesions of optic nerve and anterior

chiasm
• Relatively insensitive to ophthalmologic disorders
Pattern-reversal VEPs
• Using a shift of a checkerboard
pattern without changing luminance.
• Monocular visual stimulation
• In normal subjects, the visual
stimulus evokes a prominent
waveform with positive polarity in
the posterior head region at a mean
latency of + 100 ms (P1 or P100
wave)*.
• Most common transient VEP ab(N)
in pts with anterior visual pathway
lesions is prolonged latency of the
P100 wave.
Purpose and role
• To provide quantitative determination of visual function
through the visual conduction pathways
• To assess for clinical/subclinical lesions in the optic nerve
or anterior chiasma
Methods
• Stimulation
• Pattern-reversal VEP
• Shift of checkerboard pattern
(black-white)
• No change in luminance
• Flash VEP
• more variable results in normal
subjects
• Not as sensitive for detecting
abnormalities in visual
conduction
• Monocular testing
• Fixed distance 70-100 cm
• Focus on the center of screen
• Recording
• Electrodes: Cz,Oz,O1,O2,A1,Fz
• Full field stimulation, P100 is
maximal on Oz
• LFF 0,2-1,0 Hz
• HFF 200-300 Hz
• Sweep length 200-250 ms
• 100-200 responses are averaged
• Check Visual acuity and pupillary
size
• Pattern-reversal VEP:1-2 Hz
• Freq & size of checks affect
latency
Factors affecting VEP responses
• Visual acuity

• Pupillary size

• Age, gender

• Patient cooperation

• Sedation and anesthesia

Interpretation of VEPs
• Identification of amplitude and latency of P100
• Abnormalities in VEP latencies are much more
important diagnostically
• VEP changes are nonspesific the finding of
prolonged latencies suggests a demyelinating
process
Latency (ms)
Age, year
Females Males
< 60 < 115 <120
≥ 60 <120 <125
LOCALIZATION OF LESIONS
Anterior Visual Pathway
Ab(n)  a visual conduction defect anterior to the optic
Unilateral chiasm
P100

Ab(n)
interocular  an optic nerve lesion on the side of increased value
difference in
P100 latency
(both P100
values (N)
Bilateral Bilateral optic nerve lesions
increased
P100 latency Chiasmatic lesion

Bilateral retrochiasmatic lesions