(Investigative Ophthalmology and Visual Science. 2001;42:1342-1348.)
© 2001
by The Association for Research in Vision and Ophthalmology, Inc.
Multifocal ERG Findings in Complete Type Congenital Stationary Night Blindness
Mineo Kondo1,
Yozo Miyake1,
Nagako Kondo1,
Atsuhiro Tanikawa1,
Satoshi Suzuki1,
Masayuki Horiguchi2 and
Hiroko Terasaki1
1 From the Department of Ophthalmology, Nagoya University School of Medicine; and
2 Department of Ophthalmology, Fujita Health University School of Medicine, Toyoake, Japan.
 |
Abstract
|
|---|
PURPOSE. To study the multifocal electroretinogram (mfERG) in patients with the
complete type of congenital stationary night blindness (cCSNB), which
is thought to be due to a defect in neurotransmission from the
photoreceptors to the ON-bipolar cells.
METHODS. mfERGs were recorded with the VERIS recording system from four patients
with cCSNB, none of whom had nystagmus. The stimulus array consisted of
61 hexagons, and the total recording time was approximately 4 minutes.
The amplitudes and implicit times of the first- and second-order
kernels of the local responses were compared with those from 20 myopic
controls. Waveforms of the summed response from all locations were also
compared between the two groups.
RESULTS. The first-order kernels of the mfERGs of cCSNB patients had normal
amplitudes but delayed implicit times for nearly the whole field
tested. The second-order kernel was severely attenuated in amplitude in
cCSNB patients. The ratios of the second- to first-order kernel
amplitudes were significantly reduced in cCSNB and clearly separated
the cCSNB group from the control group without any overlap of the
values.
CONCLUSIONS. The second-order kernel, which is involved in adaptative mechanism of
the retina to repeated flashes, is selectively reduced in cCSNB. The
delay of the implicit times of the first-order kernel in patients with
cCSNB may be related to the severe amplitude reduction of the
second-order kernel.
 |
Introduction
|
|---|
The Schubert-Bornschein type of congenital stationary night
blindness (CSNB) is a nonprogressive retinal disorder characterized by
night blindness, moderately decreased visual acuity, and
myopia.1
The electroretinograms (ERGs) in patients with
CSNB are quite characteristic; when elicited by a bright stimulus after
dark adaptation, the ERGs are the negative-type with an a-wave of
normal amplitude and a b-wave that is smaller than the a-wave.
Rhodopsin density and kinetics have been shown to be normal in patients
with CSNB.2
Thus, the defect in this disorder is thought
to lie not in the photoactivity in rod photoreceptors but in the
neurotransmission from the rods to the rod bipolar cells.
CSNB has been subdivided into two clinical entities: the complete type
(cCSNB), which has no detectable rod function, and the incomplete type
(iCSNB), which has a small but detectable rod function.3
4
Recent genetic analyses have shown that these two types have separate
genetic loci on the chromosome, supporting the idea that they are
distinct clinical entities.5
6
7
8
The cone pathway is also thought to be affected in CSNB. The amplitude
of the photopic ERG b-wave elicited by a brief flash is reduced in
cCSNB.9
10
In addition, when a long-duration photopic
stimulus is used, cCSNB patients show severely reduced ON-response
b-wave, whereas the OFF-response d-wave is
preserved.11
12
13
This waveform can be simulated in the
monkey photopic ERG after treatment with 2-amino-4-phosphonobutyric
acid, which blocks neurotransmission from photoreceptors to the
ON-bipolar cells.14
15
16
This implies that the defect in
the cone pathway of cCSNB also lies in the signal transmission from the
cone photoreceptors to the depolarizing ON-bipolar
cells.12
13
The multifocal ERG (mfERG) is a relatively new objective test designed
to study local retinal function.17
18
This technique
allows the simultaneous recording of focal cone ERGs from multiple
retinal locations in a single recording session of approximately 4 to 8
minutes. This technique is particularly useful when one wants to detect
local retinal damage or to assess retinal function topographically in
both normal subjects and patients with retinal
diseases.19
20
21
22
23
24
25
26
27
28
29
Although numerous researchers17
18
19
20
21
22
23
24
25
26
27
28
29
have been assessing
retinal function in various retinal diseases using the mfERG, the exact
origin of each component of the mfERG is still under investigation.
There is recent evidence that the negative and positive components of
the first-order kernel of mfERG behave as do the a-wave and the
positive peaks of the conventional full-field flash cone
ERG.21
23
In addition, by use of glutamate analogs in
rabbits, Horiguchi et al.30
demonstrated that the
first-order kernel of the mfERG contains significant contribution from
postreceptoral ON- and OFF-components as do the conventional flash cone
ERG,16
31
supporting the results of Hood and
coworkers. The second-order kernel, the temporal nonlinear
component of the mfERGs, is interpreted to be involved in short-term
adaptational mechanisms of the retina to successive flashes and
contains a greater contribution from the proximal
retina.20
23
30
32
33
34
The aim of the present investigation was to extend these previous
studies in establishing the retinal origins of each component of the
mfERG. We examined how the waveform of the first- and second-order
kernels of the mfERGs is changed in patients with cCSNB.
 |
Methods
|
|---|
Subjects
From the patients with cCSNB seen in our clinic (Department of
Ophthalmology, Nagoya University School of Medicine), four cooperative
patients were recruited and examined. None of them had nystagmus or
irregular eye movements before and during the mfERG recordings. The
clinical characteristics of the four patients are summarized in Table 1
. Patients 1 and 2 are siblings and were classified as autosomal
recessive, patient 3 as an X-linked, and patient 4 as an autosomal
recessive cCSNB. Only the eye with the better visual acuity was tested.
The corrected visual acuity ranged from 0.3 (20/67) to 0.6 (20/33), and
the refractive error from -4.00 to -9.50 diopters (D) with a mean of
-6.50 D.
Each patient was diagnosed as having cCSNB, based on ophthalmological,
psychophysical, and electrophysiological
examinations.3
4
11
All patients had poor night vision,
and no fundus abnormalities were seen except for myopic changes. The
rod branch of the dark adaptation curve was missing on psychophysical
dark adaptometry. The full-field ERGs recorded from the four cCSNB
patients are shown in Figure 1 . The rod responses were undetectable. The rod and cone mixed maximal
ERGs had a negative-shaped ERG with no oscillatory potentials. The
brief-flash cone responses presented a wide a-wave trough, and the cone
b-wave was reduced by 30% to 45%. The amplitude ratio of the cone
b-wave to the a-wave was reduced (range of cCSNB, 1.101.35; lower
limit of normals, 1.41). The amplitude of the 30-Hz flicker ERGs was
reduced by 10% to 35%. The photopic long-flash ERG showed severely
reduced ON-response b-wave and normal OFF-response d-wave.

View larger version (19K):
[in this window]
[in a new window]
|
Figure 1. Full-field ERGs recorded from a myopic control and four patients with
cCSNB (P1P4). After 30 minutes of dark adaptation, a rod ERG was
recorded with a blue light at an intensity of 5.2 x
10-3 cd-s/m2. A cone-rod mixed maximum ERG was
recorded with a white flash at an intensity of 44.2
cd-s/m2. A cone ERG and a 30-Hz flicker ERG were recorded
with a white stimulus of 4 cd-s/m2 and 0.9
cd-s/m2, respectively, on a background illumination of 68
cd-s/m2. A photopic long-flash (200 msec) ERG was recorded
with a light-emitting diode (peak wavelength, 566 nm) built-in contact
lens electrode at an intensity of 250 cd/m2 under a blue
background illumination of 34 cd/m2.41
|
|
For control, 20 normal subjects (age, 1938 years; mean, 27.1 years)
with myopia (refractive error, -3.00 to -8.50 D; mean, -5.15 D) were
examined. None had known abnormalities of the visual system except for
myopia, and visual acuity was 1.0 (20/20) or better. Informed consent
was obtained after a full explanation of the procedures. All studies
were conducted in accordance with the principles embodied in the
Declaration of Helsinki.
Multifocal ERGs
The method of recording the mfERG has been reported in detail
previously.17
18
19
20
21
22
23
24
25
26
27
28
29
In brief, mfERGs were recorded with a
VERIS recording system (EDI, San Mateo, CA). The visual stimulus
consisted of 61 hexagonal elements scaled in size to give approximately
equal amplitude mfERGs with eccentricity. The stimulus array was
displayed on a high resolution CRT monitor (SONY GDM, Tokyo, Japan)
driven at a 75-Hz frame rate. At a viewing distance of 27 cm, the
diameter of the stimulus array subtended approximately 60°. The
luminance of each hexagon was independently modulated between black
(3.5 cd/m2) and white (138.0
cd/m2) according to a binary m-sequence at 75 Hz.
A small red fixation spot was placed at the center of the stimulus
matrix. The luminance of the surround was set at 70.8
cd/m2.
Before the recording, the subjects pupil was fully dilated with a
combination of 0.5% tropicamide and 0.5% phenylephrine hydrochloride,
and the cornea was anesthetized with proparacaine hydrochloride. ERGs
were recorded with a Burian-Allen bipolar contact lens electrode
(Hansen Ophthalmic Laboratories, Iowa City, IA), and a ground
electrode was attached to the earlobe. After insertion of the contact
lens electrode, the subject was optically corrected for the viewing
distance. The opposite eye was occluded.
The signals were amplified (100,000x), and the band-pass filter was
set at 10 to 300 Hz (Grass, Quincy, MA). The sampling rate was 1200 Hz
(interval, 0.833 msec). The m-sequence used in this study had
214 elements and required a total recording time
of approximately 4 minutes. For the comfort of the subjects, the
recording time was divided into eight segments. The first- and
second-order kernels were analyzed with VERIS 2.05 software (EDI).
An artifact reduction technique was used once to improve the
signal-to-noise ratio for all subjects.17
A small amount
of spatial filtering was also applied in one patient (P3) because his
local responses were relatively noisy and the exact amplitude and
implicit time at each location could not be made; each individual
response was averaged with 6% of its six neighboring responses.
 |
Results
|
|---|
First-Order Kernel of Local Responses
Figure 2
shows the 61 first-order kernels of the local responses from a
representative myopic control (age, 20 years; refractive error, -6.00
D) and four patients with cCSNB. At first glance, it is difficult to
distinguish the patients from the myopic control; both the amplitudes
and waveforms of each local response appear similar. The amplitudes of
the local responses of the myopic controls and the patients with cCSNB
were often slightly smaller than nonmyopic normals. Because there is
electrophysiological evidence that moderate-to-high myopia causes
depression of cone function in the posterior pole of the
eye,35
36
the slight amplitude reduction was considered to
be due to the myopic changes.

View larger version (29K):
[in this window]
[in a new window]
|
Figure 2. Sixty-one local first-order kernels of the mfERGs recorded from a
myopic control (age, 20 years; refractive error, -6.00 D) and four
patients with cCSNB (P1P4).
|
|
We next assessed the local cone function quantitatively for two
parameters, viz., the amplitude and timing for the four cCSNB patients.
The amplitudes and implicit times of the positive component were
measured at all 61 locations as shown at the top of Figure 3
. As limits of normality, the 5 percentile and 95 percentile values were
obtained for the 20 myopic controls at each location. In Figure 3
, the
white areas indicate that the values of the amplitude or implicit time
were within the 5 percentile to 95 percentile range. The black areas
indicate low amplitudes or delayed implicit times greater than this
normal range.

View larger version (31K):
[in this window]
[in a new window]
|
Figure 3. Topographical map of the amplitudes and implicit times for four
patients with cCSNB. White areas: values are within 5
percentile to 95 percentile range; black areas: low
amplitudes or delayed implicit times greater than this normal range.
Note that there are regional variations on both the amplitude and
implicit time of the mfERG across the retina for normal subjects. The
normal ranges of the amplitude and implicit time were calculated at all
locations independently.
|
|
Three of the four CSNB patients (P2P4) had normal amplitudes at all
locations tested. Only one patient (P1) had reduced amplitudes in 11
areas of the nasal field. In contrast, all four CSNB patients had
delayed implicit times in many areas. Note that one patient (P4) had
normal amplitudes with delayed implicit times at all 61 locations. Of
the total 244 retinal areas tested (61 locations x 4 patients),
210 areas (86%) had significantly delayed implicit times, whereas only
11 areas (5%) had reduced amplitudes. These findings indicate that the
pathology of cCSNB affects the mfERG implicit times in preference to
reducing the amplitude.
We also examined whether there were any topographical variations in the
degree of implicit time delays with retinal eccentricity, between the
upper/lower or nasal/temporal retina, but no significant variations
were found in cCSNB.
Waveform Change of First-Order Kernel
To compare the waveforms of the cCSNB patients and the
myopic controls, the 61 local responses were summed. The superimposed
and averaged response waveforms for the 20 myopic controls are shown on
the left of Figure 4
, and the waveforms for the four cCSNB patients are shown on the right
of Figure 4
. The vertical dashed lines are drawn at 30 msec. The
results of statistical comparisons for the two groups are presented in
Table 2
. The amplitudes of the initial negative (N1) and following positive
component (P1) were not significantly different in the two groups. The
amplitude ratio of P1 to N1 also did not differ significantly between
the two groups. It was surprising that the mean amplitude of P1 was
equal to or even slightly larger in the cCSNB patients than in myopic
controls (Table 2
and Fig. 4
), which was in contrast to the results of
conventional full-field cone ERGs (Fig. 1)
. The implicit times of N1
and P1 were significantly delayed (P < 0.05,
nonparametric MannWhitney test).

View larger version (28K):
[in this window]
[in a new window]
|
Figure 4. Summed first-order kernel responses for all 61 local responses for 20
myopic controls (left) and four cCSNB patients
(right). All responses were superimposed in the
upper traces and averaged waveforms are presented in the
lower traces.
|
|
In addition to the timing delays for the N1 and P1 components, we also
noticed other minor differences in the later components. First, the
second negative component (N2) was less prominent in the responses from
the cCSNB patients (arrowhead in lower right panel of Fig. 4
). Second,
the two or three oscillations (asterisks) followed by N2 component were
diminished or essentially absent in cCSNB. Similar minor waveform
changes in the late components of the mfERGs have been reported in some
patients with diabetic retinopathy.28
It is known that the
later portion of the first-order kernel contains contributions from
second- and higher-order kernels and thus reflects the nonlinear
temporal interactions between flashes, as do the higher order
kernels.23
Second-Order Kernel
Figure 5
shows the 61 local responses of the first slice of the second-order
kernel for the same myopic control and four cCSNB patients shown in
Figure 2
. Because the second-order kernel is relatively small when
compared with the first-order kernel, it is often difficult to identify
each positive or negative component at local areas even for the
controls. It is evident, however, that the local responses of the
second-order kernel are severely reduced or virtually absent in the
four cCSNB patients. Only one patient (P4) had detectable local
responses in some regions in the upper and nasal fields, but these
responses were still smaller than those of the controls.

View larger version (22K):
[in this window]
[in a new window]
|
Figure 5. Sixty-one local second-order kernels of the mfERGs recorded from same
subjects as shown in Figure 1
: a myopic control and four patients with
cCSNB.
|
|
To compare the waveforms, all the 61 second-order kernels were summed
and the summed kernels are presented in Figure 6A
. As in Figure 4
, the superimposed and averaged response waveforms for
20 myopic controls are shown on the left, and the waveforms for the
four cCSNB patients are shown on the right. The amplitude of the summed
second-order kernel in cCSNB patients was markedly reduced as opposed
to the normal amplitudes of the first-order kernel. The amplitudes of
the second negative component (N2), the most prominent component in the
second-order kernel, were measured as shown in the left side of Figure 6B
, and the mean value was found to be significantly reduced by more
than half of the control amplitude (Table 2)
.

View larger version (25K):
[in this window]
[in a new window]
|
Figure 6. (A) Summed second-order kernels across all 61 local
responses for 20 myopic controls (left) and four cCSNB
patients (right). All responses were superimposed in the
top trace and averaged waveforms are presented in
the bottom trace. (B) Amplitude ratio of the
second- to first-order kernel for 20 myopic controls and four cCSNB
patients. Note that the ratio is significantly lower for cCSNB than for
myopic controls, and the ratio separates the two groups without any
overlap.
|
|
Because it is known that the amplitudes of the mfERGs have fairly large
intersubject variation, one of the effective ways to measure the
relative amplitude of the second-order kernel was to calculate a ratio
of the amplitudes of the second- to first-order kernels for each
subject.37
We calculated this ratio and found that it was
significantly reduced in all cCSNB patients (Table 2)
, and a plot of
the ratios separated the two groups clearly without any overlap (Fig. 6B)
.
 |
Discussion
|
|---|
Waveform Changes of First- and Second-Order Kernels in cCSNB
The results demonstrated that the cCSNB patients had two distinct
mfERG waveform changes: (1) normal amplitude with delayed implicit
times for the first-order kernel and (2) severe amplitude reduction for
the second-order kernel. These waveform changes were present for nearly
the whole field tested for all four cCSNB patients. However, they do
not appear to be specific for cCSNB because a recent
study23
reported that some patients with retinitis
pigmentosa and diabetic retinopathy have similar mfERG waveform
changes. In addition, we have observed that some patients with X-linked
retinoschisis also have similar waveform changes (unpublished
data, 2000). It is unlikely that all these patients with
different diseases have a common defect in the retinal ON-pathway as do
the patients with cCSNB.
There are two findings showing that the two waveform changes, delayed
first-order kernel and reduced second-order kernel, are related. First,
the second-order kernel contributes to the later portion of the
first-order kernel, and its contribution begins earlier than the peak
of the positive component (P1).23
Thus, the change in the
second-order kernel can affect the timing of the first-order kernel.
Second, it has been reported that large, but delayed, first-order
kernels seen in some patients are always associated with reduced
second-order kernels.23
Hood23
demonstrated
that this holds true consistently both within patients and for patients
with various diseases. Therefore, the most plausible interpretation of
the waveform changes in cCSNB is that the second-order kernel, which is
involved in adaptative mechanisms of the retina to successive flashes,
is reduced in cCSNB, presumably because of the abnormality in
postsynaptic ON pathway, and this reduced second-order kernel may cause
delayed implicit times for the first-order kernel.
Comparison with Conventional Full-Field ERG
It is currently accepted that the N1 and P1 components of the
mfERGs are comprised of the same components as the a- and the positive
waves (b-wave and OPs) of the conventional full-field cone
ERGs.21
23
30
However, it is still unknown to what extent
the N1 and P1 components of the mfERGs are correlated with the a- and
b-waves of the conventional cone ERGs in clinical diseases. In our
cCSNB patients, the b-wave of the full-field cone ERGs was reduced by
30% to 45% (Fig. 1)
, as has been previously
reported,3
9
10
but the P1 component of the first-order
kernel was not reduced. Another discrepancy between the two waveforms
is in the ratio of the amplitudes of the positive to negative
components. Although the amplitude ratio of the b-wave to the a-wave
for full-field cone ERGs is clearly reduced in CSNB (Fig. 1)
, the
amplitude ratio of the P1 to N1 of the mfERGs was equal or even
slightly larger than in the myopic controls (Table 1
and Fig. 3
). These
results suggest that, although the N1 and P1 of the mfERG may originate
from same retinal elements as the negative and positive components of
conventional cone ERG, the two waveforms are not necessarily correlated
quantitatively in retinal diseases. This disparity is thought to be
mainly due to different stimulus intensities and adaptational states
between the two stimulus conditions.21
Our present results of delayed implicit times without an amplitude
reduction for the first-order kernel are reminiscent of a previous
report of 30-Hz flicker ERG analysis in cCSNB. Kim et
al.38
reported that cCSNB patients had a phase delay in
the fundamental component of strobe-flash 30-Hz flicker ERG without
significant amplitude reduction. Although the fundamental component of
the 30-Hz flicker ERG was not analyzed in our patients because of our
recording conditions, this agreement suggests that the defect in cCSNB
causes similar waveform changes of both the fundamental component of
30-Hz flicker ERG and first-order kernel of mfERG. This implies that
there is a possibility that an interaction of the ON- and
OFF-components, which is observed in primate flicker
ERG,38
39
40
may be involved in shaping the first-order
kernel of the mfERGs.
Clinical Implications
Finally, we would like to emphasize again the importance of
measuring the implicit times of the mfERG.22
25
26
28
29
cCSNB is a nonprogressive retinal diseases characterized by night
blindness, decreased visual acuity and myopia. Fundus findings are
usually normal except for myopic changes. The diagnosis of cCSNB is not
difficult if patients visit ophthalmologists with complaints of night
blindness. However, it is known that cCSNB patients often visit
ophthalmologist only with complaints of low visual acuity or myopia.
Actually, in our hospital, the most common complaint for cCSNB at the
initial visit is not night blindness but decreased visual acuity. If
ophthalmologists do not realize the possibility of cCSNB, they may
order mfERG testing to assess central retinal function in these
patients. Then if they are not aware of the timing delay of the mfERGs,
they may conclude that cCSNB patients have normal retinal function
across whole field tested and may misdiagnose them as having amblyopia,
optic nerve or central nervous system disease, or a psychological
visual loss.
 |
Acknowledgements
|
|---|
The authors thank Donald C. Hood for valuable discussions and
comments on the manuscript.
 |
Footnotes
|
|---|
Supported by Grant-in Aid 11470363 from the Ministry of Education,
Science, Sports and Culture, Japan.
Submitted for publication July 11, 2000; revised October 30, 2000 and
January 18, 2001; accepted January 26, 2001.
Commercial relationships policy: N.
The publication costs of this article were defrayed in part by page
charge payment. This article must therefore be marked
"advertisement" in accordance with 18 U.S.C.
1734
solely to indicate this fact.
Corresponding author: Mineo Kondo, Department of Ophthalmology, Nagoya
University School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya
466-8550, Japan. kondomi{at}med.nagoya-u.ac.jp
 |
References
|
|---|
-
Schubert, G, Bornschein, H. (1952) Beitrag zur Analyse des menschlichen Electroretinogram Ophthalmologica 123,396-413[Medline][Order article via Infotrieve]
-
Carr, RE, Ripps, H, Siegel, IM, Weale, RA (1966) Rhodopsin and the electrical activity of the retina in congenital night blindness Invest Ophthalmol 5,497-507[Abstract/Free Full Text]
-
Miyake, Y, Yagasaki, K, Horiguchi, M, Kawase, Y, Kanda, T. (1986) Congenital stationary night blindness with negative electroretinogram: a new classification Arch Ophthalmol 104,1013-1020[Abstract]
-
Miyake, Y, Horiguchi, M, Suzuki, S, Kondo, M, Tanikawa, A. (1997) Complete and incomplete type congenital stationary night blindness as a model of "OFF-retina" and "ON-retina." LaVail, MM Hollyfield, JG Anderson, RE eds. Degenerative Retinal Diseases ,31-41 Plenum Publishing New York.
-
Strom, TM, Nyakatura, G, Apfelstedt-Sylla, E, et al (1998) An L-type calcium-channel gene mutated in incomplete X-linked congenital stationary night blindness Nat Genet 19,260-263[Medline][Order article via Infotrieve]
-
Bech-Hansen, NT, Naylor, MJ, Maybaum, TA, et al (1998) Loss-of-function mutations in a calcium-channel 1-subunit gene in Xp11.23 cause incomplete X-linked congenital stationary night blindness Nat Genet 19,264-267[Medline][Order article via Infotrieve]
-
Bech-Hansen, NT, Naylor, MJ, Maybaum, TA, et al (2000) Mutations in NYX, encoding the leucine-rich proteoglycan nyctalopin, cause X-linked complete congenital stationary night blindness Nat Genet 26,319-323[Medline][Order article via Infotrieve]
-
Pusch, CM, Zeitz, C, Brandau, O, et al (2000) The complete form of X-linked congenital stationary night blindness is caused by mutations in a gene encoding a leucine-rich repeat protein Nat Genet 26,324-327[Medline][Order article via Infotrieve]
-
Krill, AE, Martin, D. (1971) Photopic abnormalities in congenital stationary nightblindness Invest Ophthalmol Vis Sci 10,625-635[Abstract/Free Full Text]
-
Lachapelle, P, Little, JM, Polomeno, RC (1983) The photopic electroretinogram in congenital stationary night blindness with myopia Invest Ophthalmol Vis Sci 24,442-450[Abstract/Free Full Text]
-
Miyake, Y, Yagasaki, K, Horiguchi, M, Kawase, Y. (1987) On- and off-responses in photopic electroretinogram in complete and incomplete types of congenital stationary night blindness Jpn J Ophthalmol 31,81-87[Medline][Order article via Infotrieve]
-
Houchin, K, Purple, RL, Wirtschafter, JD (1991) X-linked congenital stationary night blindness and depolarizing bipolar system dysfunction [ARVO Abstract] Invest Ophthalmol Vis Sci 32(4),S1229Abstract nr 2741
-
Young, RSL (1991) Low-frequency component of the photopic ERG in patients with X-linked congenital stationary night blindness Clin Vis Sci 6,309-315
-
Knapp, AG, Schiller, PH (1984) The contribution of on-bipolar cells to the electroretinogram of rabbits and monkeys Vis Res 24,1841-1846[Medline][Order article via Infotrieve]
-
Evers, HU, Gouras, P. (1986) Three cone mechanisms in the primate electroretinogram: two with, one without OFF-center bipolar responses Vis Res 26,245-254[Medline][Order article via Infotrieve]
-
Sieving, PA, Murayama, K, Naarendorp, F. (1994) Push-pull model of the primate photopic electroretinogram: a role for hyperpolarizing neurons in shaping the b-wave Vis Neurosci 11,519-532[Medline][Order article via Infotrieve]
-
Sutter, EE, Tran, D (1992) The field topography of ERG components in man-I. The photopic luminance response Vis Res 32,433-446[Medline][Order article via Infotrieve]
-
Bearse, MA, Jr, Sutter, EE (1996) Imaging localized retinal dysfunction with the multifocal electroretinogram J Opt Soc Am A 13,634-640[Medline][Order article via Infotrieve]
-
Kondo, M, Miyake, Y, Horiguchi, M, Suzuki, S, Tanikawa, A. (1995) Clinical evaluation of multifocal electroretinogram Invest Ophthalmol Vis Sci 36,2146-2150[Abstract/Free Full Text]
-
Palmowski, AM, Sutter, EE, Bearse, MA, Jr, Fung, W. (1997) Mapping of retinal function in diabetic retinopathy using the multifocal electroretinogram Invest Ophthalmol Vis Sci 38,2586-2596[Abstract/Free Full Text]
-
Hood, DC, Seiple, W, Holopigian, K, Greenstein, V. (1997) A comparison of the components of the multifocal and full-field ERGs Vis Neurosci 14,533-544[Medline][Order article via Infotrieve]
-
Hood, DC, Holopigian, K, Greenstein, V, et al (1998) Assessment of local retinal function in patients with retinitis pigmentosa using the multi-focal ERG technique Vis Res 38,163-179[Medline][Order article via Infotrieve]
-
Hood, DC (2000) Assessing retinal function with the multifocal technique Prog Ret Eye Res 19,607-646[Medline][Order article via Infotrieve]
-
Kretschmann, U, Seeliger, MW, Ruether, K, Usui, T, Apfelstedt-Sylla, E, Zrenner, E. (1998) Multifocal electroretinography in patients with Stargardts macular dystrophy Br J Ophthalmol 82,267-275[Abstract/Free Full Text]
-
Seeliger, M, Kretschmann, U, Apfelstedt-Sylla, E, Ruther, K, Zrenner, E. (1998) Multifocal electroretinography in retinitis pigmentosa Am J Ophthalmol 125,214-226[Medline][Order article via Infotrieve]
-
Seeliger, MW, Kretschmann, UH, Apfelstedt-Sylla, E, Zrenner, E. (1998) Implicit time topography of multifocal electroretinograms Invest Ophthalmol Vis Sci 39,718-723[Abstract/Free Full Text]
-
Marmor, MF, Tan, F, Sutter, EE, Bearse, MA (1999) Topography of cone electrophysiology in the enhanced S cone syndrome Invest Ophthalmol Vis Sci 40,1866-1873[Abstract/Free Full Text]
-
Fortune, B, Schneck, ME, Adams, AJ (1999) Multifocal electroretinogram delays reveal local retinal dysfunction in early diabetic retinopathy Invest Ophthalmol Vis Sci 40,2638-2651[Abstract/Free Full Text]
-
Piao, CH, Kondo, M, Tanikawa, A, Terasaki, H, Miyake, Y. (2000) Multifocal electroretinogram in occult macular dystrophy Invest Ophthalmol Vis Sci 41,513-517[Abstract/Free Full Text]
-
Horiguchi, M, Suzuki, S, Kondo, M, Tanikawa, A, Miyake, Y. (1998) Effect of glutamate analogues and inhibitory neurotransmitters on the electroretinograms elicited by random sequence stimuli in rabbits Invest Ophthalmol Vis Sci 39,2171-2176[Abstract/Free Full Text]
-
Bush, RA (1994) Sieving PA A proximal retinal component in the primate photopic ERG a-wave. Invest Ophthalmol Vis Sci. 35,635-645[Abstract/Free Full Text]
-
Bearse MA, Sutter EE, Sim D, Stamper R. Glaucomatous dysfunction revealed in higher order components of the electroretinogram. In: Vision Science and Its Applications, Volume 1, OSA Technical Diget Series. Washington, DC: Optical Society of America; 1996:104-107.
-
Sutter, EE, Bearse, MA, Jr (1999) The optic nerve head component of the human ERG Vis Res 39,419-436[Medline][Order article via Infotrieve]
-
Hasegawa, S, Oshima, A, Hayakawa, Y, Takagi, M, Abe, H. (2001) Multifocal electroretinograms in patients with branch retinal artery occulusion Invest Ophthalmol Vis Sci 42,298-304[Abstract/Free Full Text]
-
Ishikawa, M, Miyake, Y, Shiroyama, N. (1990) Focal macular electroretinogram in high myopia [Japanese] Nippon Ganka Gakkai ZasshiActa Soc Ophthalmol Jpn 94,1040-1047
-
Kawabata, H, Adachi-Usami, E. (1997) Multifocal electroretinogram in myopia Invest Ophthalmol Vis Sci 38,2844-2851[Abstract/Free Full Text]
-
Hood, DC, Greenstein, VC, Holopigian, K, et al (2000) An attempt to detect glaucomatous damage to the inner retina with the multifocal ERG Invest Ophthalmol Vis Sci 41,1570-1579[Abstract/Free Full Text]
-
Kim, SH, Bush, R, Sieving, PA (1997) Increased phase lag of the fundamental harmonic component of the 30-Hz flicker ERG in Schubert-Bornschein complete type CSNB Vis Res 37,2471-2475[Medline][Order article via Infotrieve]
-
Bush, RA, Sieving, PA (1996) Inner retinal contributions to the primate photopic fast flicker electroretinogram J Opt Soc Am A 13,557-565[Medline][Order article via Infotrieve]
-
Kondo, M, Sieving, PA (2001) Primate photopic sine-wave flicker ERG: vector modeling analysis of component origins using glutamete analogs Invest Ophthalmol Vis Sci 42,305-312[Abstract/Free Full Text]
-
Suzuki, S, Horiguchi, M, Tanikawa, A, Miyake, Y, Kondo, M. (1998) Effect of age on short-wavelength sensitive cone electroretinogram and long- and middle-wavelength sensitive cone electroretinogram Jpn J Ophthalmol 42,424-430[Medline][Order article via Infotrieve]
This article has been cited by other articles:

|
 |

|
 |
 
K. W. Bronson-Castain, M. A. Bearse Jr, Y. Han, M. E. Schneck, S. Barez, and A. J. Adams
Association between Multifocal ERG Implicit Time Delays and Adaptation in Patients with Diabetes
Invest. Ophthalmol. Vis. Sci.,
November 1, 2007;
48(11):
5250 - 5256.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
I. V. Glybina and R. N. Frank
Localization of multifocal electroretinogram abnormalities to the lesion site: findings in a family with best disease.
Arch Ophthalmol,
November 1, 2006;
124(11):
1593 - 1600.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
C.-H. Piao, M. Kondo, M. Nakamura, H. Terasaki, and Y. Miyake
Multifocal Electroretinograms in X-Linked Retinoschisis
Invest. Ophthalmol. Vis. Sci.,
November 1, 2003;
44(11):
4920 - 4930.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
K. R. Alexander, C. S. Barnes, and G. A. Fishman
ON-Pathway Dysfunction and Timing Properties of the Flicker ERG in Carriers of X-Linked Retinitis Pigmentosa
Invest. Ophthalmol. Vis. Sci.,
September 1, 2003;
44(9):
4017 - 4025.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
K. Nagasaka, M. Horiguchi, Y. Shimada, and M. Yuzawa
Multifocal Electroretinograms in Cases of Central Areolar Choroidal Dystrophy
Invest. Ophthalmol. Vis. Sci.,
April 1, 2003;
44(4):
1673 - 1679.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
Y. Shimada and M. Horiguchi
Stray Light-Induced Multifocal Electroretinograms
Invest. Ophthalmol. Vis. Sci.,
March 1, 2003;
44(3):
1245 - 1251.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
D. C. Hood, L. J. Frishman, S. Saszik, and S. Viswanathan
Retinal Origins of the Primate Multifocal ERG: Implications for the Human Response
Invest. Ophthalmol. Vis. Sci.,
May 1, 2002;
43(5):
1673 - 1685.
[Abstract]
[Full Text]
[PDF]
|
 |
|