EDX: Evoked potentilas

God protect us

Electrodiagnosis text review

Presented by: S.Sadeqi
MD , PM&R res.
SBUMC
Jan-feb 2013

Sadeqi.shahram@gmail.com

Dumitru Chap.9
Delisa Chap.4
kimura

Historical aspects
Anatomical basis
Nomenclature
Instrument

Waveform
Technique
VEP
ABR
Clinical usage

oRichard caton
o1875
oVEP
oEEG
oABR

 1891

Avraging

 Beck

Time locked

 ABR

Evoked

Dorsal column
Lemniscal sys
Dorsal root gangilia

•Thalamocortical fibers
•SS cortex

Spinomedullothalamic
Nucleos Z

VPL

nomenclature
AES

standarde electrode site
waveform
morphologic nomenclature
instrumentation parameters
recording practices
interpretive qualifications
reference data collection

Cephalic VS noncephalic montage

Scalp l0-20 International System
(I) electrode sites are located on the scalp by using measurements
based on a percentage of the skull's size with respect to standard
landmarks (usually 10 or 20%) and not absolute distances
(2) the entire skull is represented in the system
(3) Electrode sites are labeled according to assumed cortical
structures over which the electrodes are placed.
 After 6 months of age a full electrode complement usually can

be applied

Four standard landmarks are required to locate all

positions necessary for SEP purposes

Cz
C3 and C4

C3' and C4‘
FpZ
Fz
FpZ'

Upper Limb Stimulation
Erb’s point (EP1/EP2)

2-3 cm superior to the clavicle and just lateral to the clavicular
head of the sternocleidomastoid muscle

The Erb's point electrode defined as

E-l is ipsilateral to the stimulated limb

Cervical Spinous Process
C2S
C5S
C7S
REF:FPZ

Montage for upper limb SEP
Ch1: scalp electrode (C3' or C4')
Ch2: C3' or C4‘
Ch3: CS5 or C2S (C7S)
Ch4: ipsilateral EP

midfrontal region FpZ‘
contralateral EP
scalp's FpZ‘
contralateral EP

Lower Limb Stimulation
Popliteal Fossa
 EI electrode located over the tibial nerve approximately 4 cm

proximal to the popliteal crease midway between the tendons
of the semimembranous/semitendinous muscles medially and
the tendon of biceps femoris laterally PF
 The E-2 electrode is usually placed on the medial surface

of the knee.

Thoracolumbar Spinous Processes
L3S or L4S
E2: 4cm rostral or on controlateral Iliac crest
 Calculate the interval between PF and L3S, yielding the conduction

time from the knee to the cauda equina region
 It may be clinically relevant to obtain this potentia] in patients
suspected of having peripheral nerve lesions.

T12S or L1S
E2: placed 4 cm rostral to this location or CL iliac crest
 It is important to note that both of these spinal electrodes can be

used for both left and right lower limb stimulations

•It is important to recognize that the lumbosacral spine potentials

may normally be unobtainable in older or obese persons, and at
times in healthy young individuals; hence absence of the response
should not be considered abnormal.

Scalp for lower limb SEP
2 cm posterior to the vertex of the skull (CZ) utilizing

the 10-20 system and is called CZ‘
The same E-2 , FpZ', as that used for upper limb

Montage for lower limb SEP
CH1: CZ' referenced to FpZ‘
CH2: TI2S or LIS referenced to the electrode 4cm superior
to this location or the iliac crest
CH3: L3S or L4S referenced to the electrode placed
4 cm rostral to this location or the iliac crest
CH4: PF to medial knee

Montage for 2 channel set
Upper limb:
CH1: (C3' or C4') refrenced to EP
CH2: C2S (C5S or C7S) referenced to FpZ'

Lower limb: Para spinalis noise :/

Another possibility may be to forego the PF and one of the spine
sites, e.g., L3S. If the spinal potential is normal, PF is of
questionable value. Of course, if there is an abnormality in the
spinous process electrode chosen, it is then necessary to explore
the possibility of a peripheral nerve versus plexus lesion.
In this case, the needle electromyographic examination is
the procedure of choice in delineating the lesion and not the
SEP.

SEP WAVEFORMS
Polarity
Peak nomenclature
 AES N20/N30
Peak latency
Inter peak latency

Peak latency
A recommended practice is to always perform two separate trials

of each response to ensure reproducibility.
averaged trace obtained in the absence of a stimulus
alternate the polarity of the stimulator during data collection
Rotating the anode about the cathode

Inter peak latency

impulse's time of propagation between recording sites
central conduction time
EP and PF are the markers of peripheral nerve function

Amplitude measurment
side-to side amplitude differences of 50% or more are

considered indicative of a possible abnormality.
 It must be recognized, however, that normal persons can have
considerable side-to-side amplitude differences, approaching
80% or more

Base to peak VS peak to peak
 maxima of consecutive SEP peaks of opposite polarity
 mixing apples and oranges

WAVEFORM MORPHOLOGY
the shape of SEP waveforms is not heavily weighed in the
criteria to decide if a particular waveform should be described
as abnormal

ELECTRODES
Silver
Gold
Tin
Platinum

stainless steel
 stainless steel
 Platinum
 mixed with another metal

Skin preparation
It is generally accepted that abrasion is
considered sufficient when the impedance
measured across two such electrode
preparation sites is between 1000 and
5000 ohms Ω .

 Short period 1-2 hr
 Longer than 2hr

So which one is better? Needle or surface?
needle electrodes can have higher impedances than surface electrodes.

Once the skin is abraded sufficiently, an impedance of 2000

Ω can easily be achieved with surface electrodes. Needle
electrodes usually have impedances greater than 3000 Ω and
can even reach 10,000-13,000 Ω Ω
 risk of infection
 Discomfort
 higher electrical noise
 ease of pulling out

Concerns regarding contamination with the HIV and the
hepatitis virus are similar for both needle and surface electrodes.

Any electrode, surface or needle, potentially exposed to

Creutzfeldt disease or other possible slow virus disorders should
be safely and immediately discarded.

In the only study to compare scalp recorded SEPs utilizing surface
and needle electrodes, no statistically significant difference was
detected between waveform latency and amplitude.

. . . So;
use needle electrodes only on the scalp and place surface cup
electrodes at all other recording locations.

STIMULATING ELECTRODES
stimulus pulse of 200--300 µS Duration
Sensory threshold is defined as the current intensity

when the patient first describes a sensation resulting
from the stimulating pulse.
Raising' the current intensity to 2.5-3.5 times this
value, given patient tolerance, should suffice in producing a
clearly defined sensory SEP.
A moderately vigorous twitch

Suboptimal stimulus delivery
delayed arrival
smaller amplitude
Unexpected morphology

A good judge of an adequate stimulus for mixed nerve

studies is observing an adequate muscle twitch

Analysis time:
UL: 50 ms 20 HZ ≠ 5 HZ ≠ 5.1
LL: 100 ms 10 HZ ≠ 2-3 Hz ≠ 2.8
In both upper and lower limb investigations, the rate of
stimulation should not be an integral of 60 Hz so as to
minimize recording this common environmental noise

Averaging
To improve S/N ratio
To have good signal analysis , in theory the time
sampling rate must be at least twice the highest
frequency of the EP signal that is to be recorded.

Be ware of events that are not directly triggered
by stimulus, but repaeted or time locked signals:
Line current noise
Regular brain wave rhythm
Stimuls induced filter

Amplifier ringing
Myogenic synchronous movements

PATIENT COOPERATION
PATIENT HEIGHT
AGE
GENDER

TEMPERATURE
MEDICATION
SLEEP

Height
When considering central conduction times for median nerve

excitation, N13 to N20 inter-peak latency, there appears to be
little correlation with arm length or height
The lumbar N20 to cortical P37 (P40 as designated by some
authors) inter-peak latency (central conduction time) for tibial
nerve stimulation, however, is correlated with an individual's
height

Age
Cortical SEP Amp : U shaped curve
Spinal SEP: infant> the others
Unlike age-related amplitude effects, the correlation

between age and conduction time (conduction velocity) is
less clear.
peripheral nervous system initially demonstrates slow
conduction velocities until about 4 or 5 years
of age, at which time adult values are achieved
Adult SEP conduction values are usually achieved
between 5 and 8 years of age

A final consensus regarding the effects of aging on central
conduction is not yet at hand, but there appears to be a small
central conduction velocity declinein persons over 60 years of age.

0.3 ms/yr

gender
prolongation of potential latencies in men

The central conduction time appears to bear no

relationship to the gender of the subjec sex

Enviro. Temp.
Surface temperature of the upper limb at or proximal to the site

of nerve stimulation should be maintained at 32°C or more, while
the lower limb should be approximately 30°C or higher
 Central core temperature is subject to less fluctuation with

respect to emotional or environmental conditions
omeasuring latencies in patients with fevers (38.0-39.7°C) and

again following fever resolution.
oNo significant latency changes were noted in these patients
 Over 42 ‘c: no obtainable SEP
 Below 29: amp dec. And pro L.

Medication
Phenobarbital : no effect
Phenytoin: Latency prolonged. AMP fix
CMZ and pirimidone: no effect
Diazepam: no effect, hypnotic effect, dec. Muscle artifact
 the volatile agents in high concentrations such as the halogenated

hydrocarbon inhalation agents (halothane, enflurane, and
isoflurane) produce an increase in cortical potential latencies in
addition to a reduction in cortical potential amplitudes and
central conduction time us prolonged.

These effects are countered by employing a balanced

anesthesia technique that uses a strong narcotic in addition
to a muscle relaxant plus a weak anesthetic like nitrous
oxide or low concentrations of isoflurane.

sleeeeeeee

p

In general, sleep tends to reduce the amplitude and

increase the latencies of recorded SEPs

Far field and near filed potentials

Size changes producing farfield potentials.

SEP waveform neural-generators

Spinal pathway
In patients with multiple sclerosis
presenting with alterations in
vibration and proprioception,
namerow found that these
individuals had abnormalities of
their SEPs in proportion to the
clinical loss of these particular
clinical modalities
(proprioception and vibration).

in persons with clinical evidence of thalamic pathology, the
SEPs were clearly abnormal, whereas those patients with brain
stem lesions not involving the lemniscal fibers had normal SEPs.

dorsal columns impulses generating the SEP.

Good correlation was obtained between the clinical

examination and abnormal SEPs, implying that the SEP
directly correlated to both the dorsal column pathway
and the modalities of vibration and proprioception.

Upper limb SEP
EP: N9/10
Plexus

 it is absent in patients with lesions of the brachial plexus but present

in patients with cervical root avulsions

•Motor fibers are involved, too!

Upper limb SEP
C2s, C5s, C7s
 N11:

 dorsal root E.zone
 DCV

 The refractory period of this waveform is short

Hypothermia studies demonstrate an increase of the waveform's

amplitude similar to that found in peripheral nerves

Upper limb SEP

N13:
Stationary pot.
 relatively long refractory period, suggesting the involvement of

synaptic transmission

cervical cord's dorsal gray matter

Upper limb SEP

N13a: dorsal gray of the cervical cord
N13b: cuneatus N.
hypothermia reduces the amplitude of this waveform,
suggesting that synaptic transmission is involved in
its production

Upper limb SEP

N14:
Medial lemniscus

 N13 and N14 peaks likely represent generators
below and above the foramen magnum.

Upper limb SEP

Scalp:
N19/20
N18: thalamus
Various lesions in patients with thalamic pathology support the

view that the l8-ms negative peak is associated with the
thalamus or its projections to the cerebral cortex.

Lower limb SEP

PF
N7-10

Lower limb SEP
Third Lumbar Vertebra
N17-21
A short refractory period suggests that synaptic relays are not

associated with the propagation of this wavefront from the lower
limb to the thoracic aspects of the spinal cord.

cauda equina

Lower limb SEP
Twelfth Thoracic Vertebra
N22

Long refractory period: 6-10 ms
Synaptic transmission

dorsal gray's interneuronal population of cells
associated with the root entry zone of the tibial nerve's
compartment fibers in the caudal portion of the spinal
cord

Lower limb SEP
Farfield
satationary P.
On T12 level
at N22

Lower limb SEP
Second Cervical Potential
N29
Stationary potentials

oA rather long refractory period is noted for this cervical

potentiaI

nucleus gracilis

Lower limb SEP
Scalp
P37/N45

The amplitude of the cortical waveform is slightly larger

over the ipsilateral scalp

postcentral gyrus area of the cortex

Contravercy!
neural generators
Variability of latencies and amplitudes
reference data
Appropriate applications

1- Stimulating of mixed peripheral nerve and recoding from spine
and scalp
2- Stimulating a pure sensory nerve (Segmental SEP) *
3- Dermatomal SEP, not involving nerve trunk *

* Beacuse of very low Amp.

Response in the 2nd and 3rd category

Surronding muscles and inviromental noise
Only scalp recording be performed
 segmental stimulation results in more easily obtainable and somewhat

larger responses than dermatomal SEPs, as more nerve fibers are excited.

Mixed nerve SEP
median nerve

1- Erb point: N10
2- C2S, C5S, C7S : N13
3- Scalp: N20
 Analysis time : 50 ms
 Between 300 – 1000 Av.

Central conduction time
(N 13-N20 latency)
demonstrating a mean conduction time of 5.6 ms
EP = 0.086H + 0.038A - 5.88 for men
EP =0.054H + 0.03A - 0.59
for women
 N13 = 0.099H + 0.045A - 4.98
 N13 = O.064H + 0.035A + 0.78

for men
for women

 N19 = 0.095H + 0.049A + 1.19

for men
 N19 = 0.085H + 0.043A + 2.72 for women

Mixed nerve SEP
ulnar nerve
Identical recording sites are used for the ulnar nerve as

those for the median nerve.
 smaller response than median N. .

Alternate recordings
 Between humeral epicondyles
 Ulnar groove or olecranon

Segmental sensory SEP
 sensory threshold : 3-4 A *2.5-3.5 = 6-12 A
 no muscle twich

 difficult recording over erb and spine

Central amplification

Upper limb segmental SSEP

1. Median: first 3 digit
2. Ulnar: 5th digit
3. SRN : 2cm proximal to radial styloid

4. LAC: 2cm lat. To BB tendon, 2 FB below anticubital crease:

injury to MC nerve or C5 root

LOWER LIMB SEPs
1- mixed nerve
2- segmental SSEP
3- dermatomal SSEP
lower limb dermatomal and segmental studies are somewhat

easier to perform than upper limb segmental SEPs
because
lower limb cortical waveforms are usually larger.

Tibial Nerve mixed SSEP
Stimulation on :
1- medial malleolus
2- PF
Recording sites ;
1- PF: as the marker for peripheral nerve function
2- L3s/L4s: quada equina
3- T12/L1: most quadal portion of the cord N22
4- Scalp P37

N22 = 0.174(H) + 0.076A - 9.2525
N22 = 0.1619H + 0.0694A - 7.5235

for men
for women

P37 (40) = 0.199H + 0.0852A + 3.8025

for M
P37 (40) = 0.2222H + 0.5995A + 1.1210 for W

 N22/P37 = 0.944H + 0.0233A - 0.2730
 N22/P37 = 0.0943H + 0.0425A - 0.2076

for M
for W

Alternaive recordings
When stimulation on PF

Recording from sciatic N.
E1: on sciatic notch
E2: greater trochanter
Fpz’
spinal cord conduction time
bilateral tibila nerve st. Be needed

 C7s-

LOWER LIMB SEGMENTAL SOMATOSENSORY EVOKED POTENTIALS
 Sural : between lat. Malleolus and achilles
SPN: between the middle and lateral thirds of this imaginary

Line Connecting the medial and lateral malleoli
 Saphenous: 1 FB anterior to med. Malleolous
A second site of stimulation is in the groove formed by the medial aspect of the
tibia and the medial gastrocnemius.
 lateral femoral cut. N. : 12 cm distal to ASIS

The clinical utility of both segmental and dermatomal studies is

unclear :|
and the relative value of either compared with the other is also
unknown :|

DERMATOMAL SOMATOSENSORY EVOKED POTENTIALS

The techniques to record dermatomal SEPs are relatively

straightforward.
 Considerable latency (up to 8-9 ms) and amplitude (80%)

side to side differences can occur in normal persons

L5 dermatomal SEP
omedial aspect of the first metatarsophalangeal joint
oon the dorsum of the foot between the first and second digit

oon the dorsum of the foot surrounding the first metatarsophalangeal joint

Stimulation:
 pulse duration of 200 µs
cathode should be located at either the level of the
first metatarsophalangeal joint along its medial aspect  rate less than 5 Hz
 2 and 3 times the
or in the
sensory threshold
web space between the first and second digit in the foot

Recording:
as other lower limb SSEP
E1 on CZ’
E2 on Fpz’
100 ms (sweep of 10 ms/div)
combined with 500 to 1000 averages

P40 = 8.3 + 22.4 (Height) + 0.086 (Age) ± 2.7 ms

S1 Dermatomal SEP
lateral margin of the foot at the fifth metatarsophalangeal joint

P(40) = 8.6 + 24.0 (Height) + 0.038 (Age)

2.9 ms

one obvious limitation of the dermatomal response
Only one recording site
No peripheral recording site
Either peripheral or central pathology in Abnolrmal SSEP

PUDENDAL NERVE SEP
 S2,3,4

 SNS: T12 and upper lumbars *

 PNS: S2-4 : Ant. Spinal nerve root : hypogastric plexus
 Sensory afferent : dorsalis penis/clitoris
 Motor: anal sphincter
oUrinary Control
oBowel Control
oSexaul Responsiviness
oPenile Erection

oEjaculation

 Stimulation:
on the shaft of penis
cathode proximal
200 µs
2-3 times folded sensory threshold
5 Hz

Recording

Scalp: CZ’ refrenced to FpZ’
Spine: L1s : usually in M, rarely in W

Clinical use
 Anal sphincter manometric abnormality W/O structural defect

Impotence or orgasmic or gynecologic disturbbances
Scaral plexus continuty
Sacral level radiculopthies
Metabolic Dis. Affecting bowel/bladder or sexual function

Unexplained perineal numbness or pian
CNS cause of anorectal dysfunction: MS,QE,SCI,ALS
Probable PN injury in pt. With Hx of pelvic surgery
Neuromyopathic/myopathic process affecting continence

more common etiologies of recurrent/chronic traction (partial)
injuries to the pudendal or perineal nerve distal motor branches
(which innervate the perineum and anus) are
Prolapse
2. dyschezia
3. Multiparity
4. forceps delivery
5. increased duration of the second stage of labor
6. a third-degree perineal tear
7. high-birth-weight children
8. prior pelvic surgery
9. chronic straining from constipation
10. the aging process.
1.

Normal values
 biphasic: pos-

neg
Pos: 37-45ms (P1 peak )
Neg: 48-60 ms (N1 peak )

Peak to peak : 1.25-5 µV for men
Women are usually smaller

 The P1 (onset ) latency for the PN-SEP is generally 6-10 ms

longer than that from the peroneal nerve response from knee
level stimulation.

Trigeminal Nerve SEP
sensory receptors
trigeminal (semilunar, gasserian) ganglion
dorsal trigeminothalamic tract
both ipsilaterally and contralaterally to the (VPL)
postcentral gyrus

Stimulation:
cathode is in contact with the angle of the mouth
anode is rested on the lower lip
pulse of 200 µs ,2-3 times sensory threshold ,2-3 Hz
stimulus artifact

Recording:
Only one channel, scalp
triphasic with an initial negative deflection C5' for left and C6' for
right trigeminal nerve stimulation
2 cm posterior to the line bisecting the ears and 10% of the total
coronal distance superior to the tragus region

Medial/lateral Plantar And Calcaneal Nerves

 the medial and lateral plantar responses should be obtained in all

normal persons, the calcaneal nerve response may be absent
because of too much impedance on the heel.

Clinical uses of evoked potentials
Coma Evaluation
Traumatic myelopathic evaluation
Intraoperative Monitoring
Sleep Disorders

Brain death
CVA
MS

Coma Evaluation

 GSC

 Brain stem reflexes
creatine kinase BB band levels in the cerebrospinal fluid

(CSF-CK)

median SEPs have the strongest evidence to suggest their utility

in predicting outcome after coma.
1.5 times the motor threshold is used.

The strongest indicator of a poor prognosis is a bilateral

absence of the short-latency cortical response with median nerve
stimulation.

Absence of a response is often defined as potentials less 0.5 µV .

$$$$$ Live or died $$$$$

 A: normal healthy person
 B: went to glory!
 C: absolutely wana live

Absolute peak latency, interpeak latency, and amplitude of the
short-latency cortical responses have not been shown to have a
strong prognostic significance.

Pitfalls:
Peripheral nerve, cervical spine, and brain stem

SensitivityVS Specificity
 Avoiding falsely predicting nonawakening
 correctly predicting nonawakening

Fatality rate in BACR among below main categories:
Hypoxic-Ischemic Coma (Adults): 100% died or PVS
Coma Due to Intracranial Bleed (Adults): 99%
Traumatic Coma (Adults) : 95%
adults in coma due to nontraumatic causes with BACRs to

median-nerve stimulation have a very poor prognosis for awakening

Traumatic myelopathic evaluation
Chance to return:
 clinically incomplete lesions
 Early partial return during first 48 hrs

preservation of even partial sensory function alone often has

been followed by return of voluntary motion
fairly good correlation between the SEP and motor function
return
early return of the SEP was usually, though not always, a
harbinger of motor recovery

Distinction between motor

and SSEP passages!

 Complete/incomplete
chronic/acute
SEP could not be obtained in about 15% of clinically incomplete

patients, yet these patients did just as well as other clinically
incomplete patients in whom the SEP was present
 there is no strong evidence to suggest that SEPs can play a

significant role in the prognosis of recovery following SCl.

It would appear, then, in the awake, cooperative patient, as
opposed to the unconscious one, a routine SEP study does not
substitute for a thorough clinical examination, which still appears to
be the best prognostic indicator.

Intraoperative Monitoring: Spine Surgery
SC malfunction rate:
1% in instrumentation
10% pedicle screw

removal of the rods within 6 hours usually resolves the problem

SSEP/ESG
The SEP is usually of larger amplitude than the ESG and

theoretically requires less averaging.
The SEP, however, has a much greater sensitivity than the ESG
to anesthetic agents, producing a dose-related amplitude decrease
and latency prolongation

What is the criteria?!
All peaks of the SEP or the MEP response disappear entirely or become

markedly smaller (less than 50%), or significant latency prolongation
(greater than 5.5 msec)
number of repeat trials over the next 5 or more minutes
Checking with the anesthesiologist
observed changes are not due to cranial volume conduction changes
Checking the stimulating circuit and recording inputs

Houston! Houston! We’ve hade a problem here!

Intra operative monitoring: Aortic/Cardiac surgery
Risk of paraplegia:
from 0.5 % in COA to 15% in TAA
 changes in SSEP after 3’ of cord ischemia
 total loss of all peaks after about 9’

 Maneuvers designed to increase both distal spinal cord blood

flow and perfusion have resulted in SEP reappearance without
postoperative neurologic deficits.

Intraoperative Monitoring: Carotid Endarterectomy
 cerebral ischemia secondary to carotid clamping
 detecting early cerebral ischemia
 identifying patients in whom a bypass shunt is required

The pathophysiologic process is the inability of the
brain to maintain appropriate electrical capabilities as it
becomes ischemic
regional cerebral blood flow greater than about 20 mL per 100g

per min: electrical activity is normal
 in the range,approximately, of 16 mL to 18 mL per 100g per

min : the SEP latency begins to lengthen, and changes
start occurring in the EEG
 At about 10 mL per 100g per min, both electrical indices are

essentially flat

VEP

Retinal photo receptors
optic nerve
Chiasma optic
optic tract
Lateral geniculate body
optic radiaion

primary visual cortex 17
Secondry 18 – 19

VEP

Recording:
Oz
O1 and O2
Refrenced to Cz
Gr on Fz
 corrective devices must been put on
No midriatic along 12hr

Room darkened
Monitor contrast at max. Availble
Cervical spine relaxed

VEP

Patterned St. : checkerboard

Unpat. St. : flushing

 eliminates the flash-stimulus problem
 reduces certain acuity and astigmatism variables

 gives more easily standardized responses

VEP

Flash or Goggle stimulators can be used
on children
with patients who are not able to maintain steady focusing
owing to behavioral or neuromuscular difficulties during operations
sedated or unconscious patients
visual acuity precludes shorter distance or larger check patterned
stimulus testing

VEP

The VEP amplitude normally is inversely proportional to check size

Distance: 70 -100 cm
Pattern reversing: 2 Hz
Check size: 2.91 mm
First both eyes together, then separateley

VEP

N 75 : 65-90
P 100 : 88-114

N 140 : up to 151

 The P100 latencies shorten during the first year of

life, reaching a plateau by 6 or 7 years of age, and then
increase gradually with age after 60 years.
 Women tend to have slightly shorter latencies.

VEP
Hemifield stimulation is used to evaluate a unilateral postchiasmal
to occipital cortex lesion

VEP

Paradox
 unilateral CVA on Lt. Occiput cortex
 Lt. Hemifield St.
 Large VEP on Lt and NL on Rt
 Rt. Hemifield St.
 Small VEP on Rt. And tiny on Lt.

The paradoxical response is observed

because the larger potential in this example,
recorded over the left occipital (i.e., O1) lobe
from left hemifield stimulation

VEP
Conditions that affect central retinal or macular function can

cause alterations in the VEP amplitude or waveform, rather than
latency, and require that a small check pattern be used
 Peripheral retinal diseases will not significantly alter the VEP

until the macula is involved
central retinal artery occlusion may not produce any VEP

abnormality
ischemic or compressive optic neuropathies can cause waveform
and amplitude abnormalities that are out of proportion to the latenvy
delay
Papilledema, in the absence of secondary ischemic atrophy, may
not give any VEP abnormalities.

VEP
Cortical blindness usually abolishes the VEP

differentiating conversion symptoms from organic lesions
MS and other demyelinating diseases giving latency

prolongations up to the 250-msec range
Toxic or nutritional amblyopias, which are considered
demyelinating, usually are not associated with significant VEP
alteration.
 Chiasmal lesions generally alter the VEP bilaterally
 Postchiasmal focal lesions are best defined with partial or

hemifield stimulation

Oto-acoustic emission
cochlear outer hair cells' vigorous motility
 superior screening of early hearing problems in infants
 for early detection of hearing loss from ototoxic drugs
 part of an assessment battery for children with auditory

processing deficits
 evaluating cochlear damage from noise exposure
 when tinnitus is part of the presenting report

Auditory brainstem response
the smallest of the EP responses
amplitude usually is no more than 600 nanovolts
o organ of Corti
o spiral ganglion
o auditory or cochlear nerve
o cochlear nuclei # 3
o lateral lemniscus
o superior olivary complex
o Medial geniculate body (4 )
o auditory cortex 41

ABR

Recording:
Active: Cz
Ref to ipsilateral earlobe (A) or mastoid bone (M)
Gr is contralateral ref. !
Otoscopic exam before test

Test room sould be free of noise or distraction
 Basic hearing treshold
 Opp. Ear masked with white noise
 Click!
 Rarefaction/condansation
 Rarefaction generally produces a shorter latency peak than

condensation when all other recording parameters are the

ABR

auditory nerve
II. cochlear nucleus at the
pontomedullary junction
III. superior olivary complex in the
caudal pons
IV. lateral lemniscus in the pons
V. inferior colliculus in the
midbrain
VI. medial geniculate body of the
thalamus
VII.auditory radiations of the
thalamocortical tract
I.

ABR

The I-III interpeak latency difference:
lesions in the peripheral auditory mechanism, auditory nerve or
lower pons level lesions

The I-V interpeak latency difference
Lesion in brainstem, thalamocortical tract
when the I-III interpeak latency is normal

Diffuse involvement both in the I-III and III-V :
MS and other demyelinating processes

ABR

ABR use in adults
unexplained central hearing losses on auditory tests
differential diagnosis of sudden-onset unilateral deafness or

severe hearing loss
detecting multiple sclerosis (MS), other demyelinating
processes, and acoustic neuromas
during cranial intraoperative monitoring (IOM)
monitoring brainstem function during barbiturate coma
brain death confirmition

ABR

ABR in children
 infants and newborns to detect the early hearing loss
considered in infants of 6 months of age or less who are
suspected of hearing loss, and in children up to 2 years of age
who appear to have hearing or behavioral problems
 prognostic considerations following hypoxic encephalopathies

Evoked potentias in MS

VEP
 The VEP abnormalities are related most

often to optic neuritis
 one usually affected more than the other
1. Prolonged P100 latency : greater than 10 to 30 msec
2. Interocular latency differences: the most sensitive indicator of

optic nerve dysfunction
3. Relative amplitude diminution:
total amplitude less than 3 µV suspicious
side-to-side amplitude difference greater than 50% abnormal
4. Dispersion or change in duration of the P100 potential
5. Other waveform morphology changes


Chronologic relation between MS and VEP
when the pattern shift VEP was normal, there was never an

abnormality found on clinical examination.
Even when the pattern shift VEP was abnormal, various clinical
examinations remained normal
when optic neuritis was clearly present, more than 95% of
patients had VEP abnormalities


ABR
Abnormal in
 30% of possible MS
 41% of probable MS
 67% of definite MS patients

1) Absence of waves, especially peak V (III)
2) Marked diminution of amplitude of the waves
3) Increased interpeak latency differences :

III-V IPL more frequently involved than the I-III
4) Reversal of I/V amplitude ratio


1. Peak latency prolongation
2. Prolongation of interpotential latency

3. Diminution of amplitude
4. Absence of component peaks
5. Change in the morphology

various combination of abnormalities


Abnormal SEP
58% for all clinical MS classifications
77 in definite MS
67% in probable MS
49% in possible MS

Abnormal evoked potentials in MS:
40% in SSEP
37% in VEP
25% in ABR


Motor cortex electrical or magnetic stimulation

cord-to-axilla conduction to be normal in both groups
whereas central conduction ( cortex-to-cord or cord-to-cord

conduction) was markedly slowed in MS patients


MRI

In brainstem lesions, the ABR is more sensitive than MRI
in optic neuritis secondary to MS, the MRI usually has been

normal, whereas pattern shift VEPs are abnormal in
approximately 95% of patients

Bradley: Neurology in Clinical Practice, 5th ed
Table 58-9

Comparison of Sensitivity of Laboratory Testing in
Multiple Sclerosis
VER BAER SSEP
OCB
MRI
80-85% 50-65% 65-80% 85-90% 90-97%

Methods for monitoring
EP recording
intracranial pressure measurement
serial EEG recording
cerebral blood flow measurement
apnea testing
ultrasound techniques

EEG findings do not correlate well with the diagnosis
of brain death
essentially a test of cortical function

In brain death, the ABR typically
has no identifiable waves,
or only isolated unilateral or bilateral wave I

can be recorded.
Only rarely is wave II present.

cases of hypoxic brain injury
Absence of a cortical SEP with preservation of the ABR

loss of cortical function
preservation of brainstem function
proceeding to a chronic vegetative state

ABR recordings in decerebration and bulbar syndromes
considerable instability
increase in the wave I latency and the interpeak latencies
Increase in central conduction time
marked peak III and V amplitude reductions

EDX: Evoked potentilas

Recomendados

Recomendados

Mais conteúdo relacionado

Mais procurados

Mais procurados (20)

Destaque

Destaque (20)

Semelhante a EDX: Evoked potentilas

Semelhante a EDX: Evoked potentilas (20)

Último

Último (20)

EDX: Evoked potentilas