VEP and its clinical importance

Presenter: Dr. Nikhil PanpaliaGuide: Dr.K.R.Naik

Introductions• VEPs (visual evoked potentials) are visually evoked

electrophysiological signals extracted from the electroencephalographic activity in the visual cortex recorded from the overlying scalp.

• As visual cortex is activated primarily by the central visual field, VEPs depend on functional integrity of central vision at any level of the visual pathway including the eye, retina, the optic nerve, optic radiations and occipital cortex

Anatomy of visual pathway

Sources of VEP

Maturation of VEP• By age three years, children can usually co-operate fully

allowing use of the same recording parameters as adults. • The problem for children less than 3 years of age is one of

maintaining fixation. • Retinal development, cortical cell density, myelination and

visual acuity are close enough to that of an adult by age 5 years, that children by this age produce adult VEP waveforms.

• “P1″ component of the flash VEP can be recorded in the full term infant within 5 weeks of age with a peak time of less than 200 msec. VEPs change rapidly in form and complexity in the first six months.

• As the infant matures this late “P1″ appears earlier and earlier so that by about age 4-5 years, peak time shortens to about 100 msec using pattern reversal stimuli, and about 110 msec using flash stimuli.

• Peak times remain at this point for most of one’s adult life with no statistically significant change until after age 55 years.

• Components of the VEP change gradually after age 55 displaying attenuation in amplitude and slowing of the P1 component.

• Thus, the two periods in life that vary most in VEP physiology are the first few years during early maturation and during aging after age 60 years.

• The amplitude of the mature P1 component of flash and pattern VEPs is greatest at about age 7-8 years.

• The brain reaches 90% of adult size as early as age 6 years. • As children enter adolescence and mature brain and scalp

tissues thicken attenuating the brain’s signal as recorded from the overlying scalp.

• The amplitude and speed of VEPs remains stable until about age 28 years at which time amplitudes begin to attenuate (Emmerson-Hanover, 1994).

Methods• Pretest evaluation

• Running the test

• Partial field stimulation

• Normal PSVEP

Pretest evaluation

• Patient co-operation

• Usual glasses if any should be put on.

• Visual acuity, pupillary diameter and field chart

• In patients with field defects lateral placement of electrode is necessary because field defects alter potential field difference of p100.

Running the test

• Standard EEG electrodes are used

• Recording electrode at Oz (inion)

• Reference Fpz

• Ground electrode at Cz

• Electrode impedence below 5killoohms

• Amplification 20,000-1,00,000 for PSVEP

Montages• Four channels recommended

• Channel 1: Oz-Fpz• Channel 2: Pz-Fpz• Channel 3: L5-Fpz• Channel4: R5-Fpz

For some lesion there is lateral shift of P100 peak. Midline recording not reliable and hence six channel machine recommended specially in hemifield stimulations.

• Channel 1: Oz-Fpz• Channel 2: Pz-Fpz• Channel 3: L5-Fpz• Channel 4: R5-Fpz• Channel 5: L10-Fpz• Channel 4: R10-Fpz

Placement of electrodes

Types of stimuli

• The checkerboard pattern is abruptly exchanged with a diffuse gray background.

• The mean luminance of the diffuse background and the checkerboard must be identical.

• Pattern onset duration should be 200 ms separated by 400 ms of diffuse background.

Pattern onset/offset stimuli

• Pattern onset: typically consists of three main peaks in adults; C1 (positive approximately 75 ms), C2 (negative approximately 125 ms) and C3 (positive, approximately 150ms)

• The flash VEP should be elicited by a brief flash that subtends a visual field of at least 20 deg, presented in a dimly illuminated room.

• The strength (time-integrated luminance) of the flash stimulus should be 3 (2.7-3.3) photopic candelas seconds per meter squared (cd·s·m-2).

• A hand held stroboscopic light or by positioning an integrating bowl (ganzfeld) .

• The flash rate should be 1 per second (1.0 Hz ±20%)

Flash stimulus

• Flash:N2 and P2 peaks,90 ms and120 ms.

• Black and white checks change phase abruptly (i.e., black to white and white to black) and repeatedly at a specified number of reversals per second.

• No overall change in the luminance of the screen,

• The large check (1°) and small check (0.25°) stimuli are specified by the check width (visual angle), the stimulus rate (in reversals per second) number of reversals, the mean luminance, the pattern contrast and the field size.

• A reversal rate of 2 reversals per second (+/- 10%) should be used to elicit the standard pattern reversal VEP.

Pattern-reversal stimuli

• The size of each check in the pattern and size of the visual field affects the VEP.

• Most laboratories initially screen patients using a video display with field subtending 10-40 degrees of arc and fairly large individual check size of about 1 degree of arc.

1. A large check size is used because most clinical laboratories are recording from patients who lack good visual acuity.

2. A person with 20/20 (6/6) or better vision will produce the largest amplitude, fastest VEP components using a small check size (a visual field comprised of checks only 5-6 mm viewed at 1 meter).

3. Each check would measure about 15-20 of arc. ′4. A person with poor visual acuity would produce the largest

amplitude, fastest components with a larger check size subtending a degree or more (such as a 20 mm check or larger viewed at 1 meter distance).

• Pattern-reversal is the preferred stimulus for most clinical purposes. Pattern-reversal VEPs are less variable in waveform and timing than the VEPs elicited by other stimuli.

• The pattern onset/offset stimulus is best suited for the detection of malingering and for use in patients with nystagmus.

• Flash VEPs are useful when poor optics, poor cooperation or poor vision makes the use of pattern stimulation inappropriate

Preferred stimuli

Technical recommendation for PSVEP

• Recording conditions:• Low cut filters 1-3 Hz and high cut 100-300 Hz. • Generally 100 epochs• Analysis Time: The minimum analysis time (sweep duration) for all adult transient

flash and pattern reversal VEPs is 250 ms and 500 ms for pattern onset/offset

• Stimulation• Black and white checkerboard or vertical grating• Contrast 50-80 %• Full field size >8 degree• Size of pattern 35-70 min• Rate: 1 Hz ( transient) and 4-8 Hz (steady)• Mean luminence central field 50 candles• Back ground lumnince 20-40 candles

About 80% of VEP occurs from central field and peripheral 8-32 degree contributes to amplitude of P100. At least two averages should be performed to verify the reproducibility of each VEP

Transient Vs steady state VEP• Steady-state VEP(3.5 Hz or more): waveform of a VEP

depends upon the temporal frequency of the stimulus. At rapid rates of stimulation, the waveform becomes approximately sinusoidal .

• Transient VEP (<3.5 Hz): At low temporal frequencies, the waveform consists of a number of discrete deflections and .

• All standard VEPs are transient

Hemifield stimulation• Complexity of PVEP can be fully appreciated with selective

visual field testing.• VEP vector tends to point obliquely to opposite hemisphere.• P100 is maximal ipsilateral to stimulus rather than

contralateral.• P100 ipsilateral (macula) N75P100N145 and N105 from

contralateral (Peripheral retina)P75N105P135. • Hemifield requires larger check size and large field

stimulation.

Full field stimuation helps to determine anterior chiasmal disorder. Hemifield stimulation is used to determine retrochaismal disorder.

• VEPs to a pattern-reversing checkerboard (the most commonly used stimulus in clinical laboratories) consist of a set of sequential waveforms .

• The waveforms are alternately positive and negative and are designated in accordance with their polarity and latency.

• Positive waves are designated P, followed by a number indicating the peak latency in milliseconds (e.g., P60 and PlOO)

• Negative waves are designated N, followed by a number indicating the peak latency N70 and NI45

VEP nomenclature

VEP

• The neural generators of the waves of the visual evoked potential (VEP) are not clearly defined.

• Research with multichannel scalp recordings, visual MRI activity and dipole modeling, supports the interpretation that the :

1. visual cortex is the source of the early components of the VEP (N1, N70) prior to P1 (“P100″) (Slotnick, et al., 1999).

2. The early phase of the P1 component with a peak around 95-110 msec, is likely generated in dorsal extrastriate cortex of the middle occipital gyrus.

3. The later negative component N2 (N150) is generated from several areas including a deep source in the parietal lobe (DiRusso et al., 2002).

P-100• Considerable variation in the morphology of normal VEPs, but the

dominant wave is the PIOO component. • Some subjects the initial negativity (N70) is absent, whereas in other

subjects N70 is as large as PIOO.

• 0.5 percent of normal cases, PlOO has a W-shaped configuration (i.e., PIOO is subdivided into two peaks).

• In these normal subjects, both peaks have latencies within the boundaries of normality.

• The best way to determine which peak corresponds to PIOO is to obtain VEPs to patterns of three different sizes. Usually the larger checks will yield only one PIOO peak

P100 morphology

• P 100 LATENCY ( m sec ) = 102 5• R-L difference ( msec) = 1.3 2.0• Amplitude (μV) =10 4.2• Duration = 63 8.7

PVEP – NORMAL DATA

LATENCY CRITERIA• PROLONGATION > 3 SD • INTEROCULAR LATENCY OF P100>10 msec, LONGER LATENCY ABNORMAL

AMPLITUDE CRITERIA• INTEROCULAR AMPLITUDE RATIO>2• ABNOMALLY LOW OR HIGH AMPLITUDE• ABSENCE OF IDENTIFIABLE VEP FROM MIDLINE AND LATERAL

OCCIPITAL SITES.

FULL FIELD PVEP- CRITERIA FOR ABNORMALITY

Principles:

• Latency prolongation: Demyelination (MS)

• Amplitude reduction: Axonal loss ( Ischemic neuropathy)

• Both: Nerve compression

Amplitude reduction

• Pupillary size

• Refractive error

• Retinal disease

• Media opacity

Variables influencing VEP• Age: Increases latency at rate of 2.5 ms/decade after fifth decade.

Attributed to changes in retina and rostral part of visual system.

• Gender: Males have longer latency because of longer head

• Eye dominace: Dominant eye have shorter latency and larger amplitude. (neuroanatomic asymmetries.

• Eye movement: Reduces amplitude without affecting asymmetry.

• Visual acuity: latency remains normal.

• Drugs: Pupillary constriction reduces latency and vice versa as does the luminence.

Multiple Sclerosis

• P latency prolongation with or without attenuation of amplitude

• Can be used to see silent lesions• Can also monitor recovery

Neuromyelitis Optica

• Un-recordable P 100 waveforms with redced amplitude.

Optic neuritis

• VEP are deformed and incomprehensible if recordable these will be prolonged in nearly all patients with optic neuropathy.

• Additional lesions in other eye to R/o Multiple sclerosis.

Ischemic optic neuropathy

• Amplitude of P100 attenuation

HIV infection

• In patients of CD4 <200 there is subclinical retinopathy. There may be reduced amplitude or prolonged latency.

Nutritional and toxic optic neuropathy

• B12 deficiency and alcoholics there is prolongation of latency.

• Normalization after treatment.

Hereditary and degenerative diseases

• Dysmyelinating disorders: Adrenolecodystrophy, metachromatic leukodystrohy and Pelizaeus-Merzbachers disease

• Heredatory optic Atrophy• CMT• Freidreich ataxia• Leber optic atrophy• Mitochondrial diseases

Compression

• Severe ICT with papilloedema: VEP unrecordable

• Pituitary tumor with Suprasellar extension: Latency prolonged.

Intraoperative testing

• Flash VEP is used• Craniopharyngioma or suprasellar tumors.• VEP shows considerable variation from

baseline surgeons should be alarmed.

Multiple sclerosis

Optic neuritis

Occipital trauma

Tumors

Ethambutol toxicity

VEP in pt TB meningitis

References

• Ebersole and Timothy A. Pedley• Visually Evoked Potentials: by Donnell J. Creel• Chiappa- Evoked potentials in medicine

Thank you