1) VEPs are electrophysiological signals extracted from the EEG activity in the visual cortex in response to visual stimulation. They provide an objective measure of visual pathway integrity from the eye to the occipital cortex. 2) VEP waveform and components mature during early childhood, peaking around ages 5-8 years, then stabilize until aging effects begin around age 55. The "P1" component can be seen in infants by 5 weeks of age. 3) Pattern-reversal stimulation with checkerboards is most commonly used clinically. It elicits a reproducible P100 component around 100ms. Hemifield stimulation can localize lesions to the pre- or retrochiasmatic regions.

1. VEP and its clinical importance
Presenter: Dr. Nikhil Panpalia
Guide: Dr.K.R.Naik

2. 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

3. Anatomy of visual pathway

7. Sources of VEP

12. 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.

13. • “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.

14. • 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.

15. • 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).

16. Methods
• Pretest evaluation
• Running the test
• Partial field stimulation
• Normal PSVEP

17. 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.

18. 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

19. Montages
• Four channels recommended
• Channel 1: Oz-Fpz
• Channel 2: Pz-Fpz
• Channel 3: L5-Fpz
• Channel4: R5-Fpz

20. 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

21. Placement of electrodes

22. Types of stimuli

23. • 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

24. • 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)

25. • 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

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

27. • 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

29. • 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).

30. • 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

31. 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

32. 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

33. 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.

35. • 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

36. VEP

37. • 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).

38. 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

39. P100 morphology

40. • 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

41. 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

42. Principles:
• Latency prolongation: Demyelination (MS)
• Amplitude reduction: Axonal loss ( Ischemic
neuropathy)
• Both: Nerve compression

43. Amplitude reduction
• Pupillary size
• Refractive error
• Retinal disease
• Media opacity

44. 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.

45. Multiple Sclerosis
• P latency prolongation with or without
attenuation of amplitude
• Can be used to see silent lesions
• Can also monitor recovery

46. Neuromyelitis Optica
• Un-recordable P 100 waveforms with redced
amplitude.

47. 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.

48. Ischemic optic neuropathy
• Amplitude of P100 attenuation

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

50. Nutritional and toxic optic neuropathy
• B12 deficiency and alcoholics there is
prolongation of latency.
• Normalization after treatment.

51. Hereditary and degenerative diseases
• Dysmyelinating disorders: Adrenolecodystrophy,
metachromatic leukodystrohy and Pelizaeus-
Merzbachers disease
• Heredatory optic Atrophy
• CMT
• Freidreich ataxia
• Leber optic atrophy
• Mitochondrial diseases

52. Compression
• Severe ICT with papilloedema: VEP
unrecordable
• Pituitary tumor with Suprasellar extension:
Latency prolonged.

53. Intraoperative testing
• Flash VEP is used
• Craniopharyngioma or suprasellar tumors.
• VEP shows considerable variation from
baseline surgeons should be alarmed.

54. Multiple sclerosis

55. Optic neuritis

56. Occipital trauma

57. Tumors

60. Ethambutol toxicity

61. VEP in pt TB meningitis

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

63. Thank you