This document provides information about visual evoked potentials (VEP) and brainstem auditory evoked potentials (BAEP). It describes how VEPs are used to assess the integrity of the visual pathway and are recorded from the scalp in response to visual stimuli. It details the anatomy of the visual pathway and different types of VEPs. It also outlines how to perform VEP testing, interpret the results, and factors that can influence VEPs. For BAEPs, it describes the auditory pathway and waves in the BAEP response. It provides details on performing BAEP testing, interpreting the results, and applications in evaluating neurological conditions.

2. Introduction
Evoked Potential:
oElectrical potentials that occur in the cortex after
stimulation of a sensory organ which can be recorded
by surface electrodes.

3. non-invasive low-cost
succession of waves or
peaks,

4. central analogies of conduction times in the
peripheral nervous system
central neural pathways.

6. Visual evoked potentials:
Electrical potentials recorded from scalp in response to
visual stimuli.
It assesses the integrity of the visual pathways from the
optic nerve to the occipital cortex.

8. ANATOMY OFVISUAL PATHWAY

9. temporal half of retina are also
situated in the temporal half of the nerve
chiasm without crossing
to ipsilateral

10. nasal half of retina are situated
in the medial half of the nerve
Decussate at chiasm
to contralateral

11. TYPES OF VEP
Pattern VEP:
oMost commonly used in clinical practice.
oFull field
oHemi field
oCentral field
oPartial field.
Flash VEP:
oLess commonly used.
oUsed in uncooperative and unconscious patients.
Chromatic patterned stimuli:
oHelpful in detecting color blindness.

13. PATIENT INSTRUCTIONS:
• Patient should be explained the test to ensure full cooperation.
• Avoid the hair spray or oil after last hair wash.
• The usual glasses if any should be put on during test.
• Avoid any mydriatic or miotic drugs 12 hr before the test.
• Results of ophthalmological examination such as visual
acuity, pupillary diameter and field charts should be reviewed
before the test.

14. HOW TO DO THE TEST ?
Equipment settings:
• Electrode impedance below 5kώ.
• Low cut filters are set at 1- 3 Hz.
• High cut filters are set at 100- 300 Hz.
• Amplification ranging between 20,000 to 100,000 is
used.
• sweep duration should range between 250 to 500 ms.

15. Procedure:
• The room should be dark.
• Test One eye at a time.
• Seating distance: 70-100 cm from the monitor screen.
• Stimulus: Checkerboard pattern (or less often, flash) is
used as stimulation.
oSkin preparation by abrading and degreasing.
oApply electrodes using jelly.

16. oElectrode placement:
oRecording electrode at Oz
(2cms above the inion).
oReference electrode at Fpz
(12cms above the nasion).
oGround electrode at Cz
(vertex).
• Fix the gaze at a colored dot in
the center of the screen.
• Check the impedance of the
electrodes and start the
averaging process.

17. • Stimulus rates of 1-2 Hz are recommended.
• Generally about 100 epochs are averaged.
• Some times 250 – 500 epochs are required to get a
clear potential.
• For judging the reproducibility of the wave forms,
these should be averaged twice and superimposed.
• Additional recording electrodes L5, R5 are used if
there is asymmetrical activation of visual cortex.

19. Waveforms (The NPN
complex)
• The initial negative peak (N1 or N75)
• A large positive peak (P1 or P100)
• Negative peak (N2 or N145)
N75
P100
N145

20. VEP generator site

21. Analysis:
• Identify the waves (NPN complex)
• Determine the absolute peak latencies
• Determine the amplitude of the waves
• Determine the inter ocular latency difference.
P-VEP normal data :
• P 100 latency: 102  5 m sec
• R-L difference: 1.3  2.0 m sec
• Amplitude: 10  4.2 μV
• Duration: 63  8.7 m sec.

22. INTERPRETATION
• Each eye projects to B/L occipital cortex via optic
chiasma.
• Unilateral VEP abnormality -
Anterior visual pathway lesion (pre chiasmal lesion).
• Bilateral VEP abnormality - No localizing value.
• Abnormalities include:
1. Latency prolongation
2. Amplitude reduction
3. Combined latency & amplitude abnormalities.

23. 1. Latency prolongation:
• P 100 Latency prolongation > 3 SD or inter
ocular latency difference > 10 m sec is significant.
• Latency depends on fast conducting fibers.
• Prolonged P 100 latency seen in demyelinating
lesions.
• Also seen in retinopathies & glaucoma.
2. Amplitude reduction:
• Amplitude of P 100 wide individual variation.
• Hence Inter ocular amplitude ratio is used to detect
abnormalities.
• Inter ocular amplitude ratio > 2 is significant.
• Reduced amplitude indicates axonal lesions( ex:
AION).

24. 3. Combined latency & amplitude abnormalities:
• Optic nerve compression produce results in segmental
demyelination and axonal loss
• Hence it produces combined latency and amplitude
abnormalities.
W shaped complex:
• It is bifid pattern of P 100 wave.
• Two peaks are separated by 10 – 50 ms.
• Rarely seen in normal individuals.
• Usually seen during field defects.

25. VARIABLES INFLUENCING
VEP
AGE-
Latency of P100 is prolonged at a rate of
2.5ms/decade after 50 years.
In infants and young children the P100 latency on
large checks reaches adult value by 20 weeks,
whereas on smaller checks takes 5-6 years to
reach adult value.

26. • GENDER
• The p100 latency is longer in adult males
compared to adult females.
• This has been attributed to larger head size and
lower body temperature in males.
• The mean amplitude is greater in females
compared to males.
• Although its basis unknown hormonal differences
have been suggested.

27. • EYE DOMINANCE
• The P100 wave obtained by stimulating dominant
eye is shorter and the amplitude is greater
compared to the nondominant eye.
• This has been attributed to neuroanatomic
asymmetries of striate cortex.
• EYE MOVEMENTS.
• Eye movement reduces the amplitude of P100
but its latency is not affected.
• Patients with nystagmus having normal visual
pathway have normal P100 latency.

28. DRUGS AND SIZE OF PUPIL
• Drugs causing pupillary constriction such as
pilocarpine can increase p100 latency which is
attributed to decreased area of retinal
illumination.
• Mydriatics have opposite effect

29. MONOCULAR ABNORMAL FULL FIELD
VEP
anterio
• Demyelination

30. BILATERAL ABNORMAL FULL FIELD PVEP

31. NEUROLOGICALAPPLICATIONSOFVEP

32. DEMYELINATING DISEAES-
MULTIPLE SCLEROSIS
the P100 latency is prolonged
with or without atentuation of amplitude
• Prolongation of p100 latency is not diagnostic of MS

33. detecting a subclinical
demyelinating plaque
more sensitive than clinical and MRI examination
of visual pathways.

34. NEUROMYELITIS OPTICA
clinically simulate MS
unrecordable p100
waveform and reduced amplitude of p100 have
been reported to be characteristic

36. COMPRESSIVE LESIONS AFFECTING ANTERIOR
VISUAL PATHWAY
• VEP in patients with papilloedema is not severe
unless there is compression of optic nerve
loss of amplitude
distortion of waveform and
prolongation of p100 latency

37. • Latency prolongation is less prolonged
is more sensitive in detecting compression of
anterior visual pathways

38. MALINGERING AND
HYSTERIA
• VEP remains normal

40. BRAINSTEMAUDITORYEVOKEDPOTENTIAL

41. of 5 waves within 10 ms
uncooperative and very young patients
severe hearing deficits.

43. starts in the cochlea
• hydrostatic pressure changes are sensed by hair
cells in the organ of Corti.

44. pontomedullary
junction via the acoustic nerve.
• second-order neurons project to ipsilateral and
contralateral superior olivary nuclei

47. BRAINSTEM ELECTRICAL ACTIVITYAND ITS
CORRELATIONWITH BAEP
WAVEFORM GENERATORS
I VIII NERVE E
II COCHLEAR NUCLEUS C
III SUPERIOROLIVARY
NUCLEUS O
IV LATERAL LEMNISCUS L
V INGERIORCOLLICULI I

48. METHOD
• RECORDING ELECTRODES-
Surface electrodes are preferred

49. Equipment settings:
• Electrode impedance below 5kώ.
• Low cut filters are set at 100 Hz.
• High cut filters are set at 3000 Hz.
• Amplification ranging between 200,000to 500,000
is used.
•

50. STIMULATION

55. WAVE I
• Patients with CNS problems only - preserved
wave I since it originates fromVIII Nerve.

56. poorly defined in some adults and most
neonates
• Prominent in contralateral channel recording

57. • Earliest component affected by pontomedullary
CVAs involving the cochlear nucleus

59. • Arises from caudal pontine tegmentum in the
superior olivary complexe

60. Bifid wave III
Poorly formed or absent wave III

61. Waves IV andV

65. MEASUREMENT & NORMALVALUES
OF BAEP

71. • Normally – 50 – 300%
• < 50% - smaller waves IV andV – Central
impairment
• >300%- small amplitude of wave I – peripheral
hearing impairment

73. As it enlarges, compress the auditory nerve

78. normal in patients with coma caused
entirely by supratentorial disease
• Abnormal BAEPs in patients with supratentorial
infarctions or hemorrhages are correlated with
poor clinical outcomes

79. • BAEPs are highly resistant to central nervous
system depressant drugs.
• BAEP is better than GCS, motor signs, EEG, CT in
predicting outcome of severe head injury

80. 35-year-old
woman who was
comatose
following a
mixed drug
overdose

81. , negative
BAEP cannot be used as evidence that the
brainstem is nonfunctional