Visual Evoked Potential (VEP) Delays in

Central Serous Choroidopathy

Jerome Sherman,* Sherry J. Bass,* Kenneth G. Noble,t Sanjeev Nath,* and Vesna Sutija*

The authors examined a series of ten consecutive patients with unilateral, idiopathic central serous
choroidopathy. Visual acuities ranged from 20/20 to 20/70 during the active stage. VEPs were recorded
to square sizes of 14, 28, and 56 min of arc. Overall, 90% of the patients had statistically significant
VEP delays from the affected eye, while only 30% had statistically significant reductions in amplitude
during the active stage. Six of the ten patients were reevaluated after the condition fully resolved. In all
six, the VEP latency returned to normal. Although the mechanism of these VEP delays is not clear,
their presence has been well documented. Therefore, a VEP delay in isolation of other tests should not
be used in the differential diagnosis of macular vs optic nerve disease. One should specifically rule out
macular disease in any patient with a delayed VEP before presuming the presence of a visual pathway
dysfunction. Invest Ophthalmol Vis Sci 27:214-221, 1986

Delays in the visual evoked potential (VEP) are
widely used to support a diagnosis of optic neuropathy
and demyelinating disease.1 VEP delays have also been
reported in other diseases, such as spinocerebellar de-
generation,2 Friedreich's ataxia,3 Parkinson's disease,4"6
vitamin B )2 deficiency,7"9 diabetes without retinopa-
thy,10 use of select drugs," 1 2 as well as in conditions
which may result in degradation of retinal images, such
as cataracts and pupillary miosis. Nevertheless, a de-
layed VEP is still considered to be the hallmark of optic
nerve demyelination.
There is a relative paucity of data, however, docu-
menting the presence of VEP delays in macular disease.
Some investigators have reported VEP phase shifts in
macular disease,13 and Lennerstrand14 has reported
abnormal VEP latencies in a majority of patients hav-
ing macular lesions. In addition, Bodis-Wollner and
Feldman 15 reported delayed transient VEPs and atten-
uated steady state VEPs in two patients with old, in-
active perimacular lesions.
We recently reported significant monocular VEP
delays in 45% of patients having either acquired uni-
lateral or asymmetric bilateral maculopathy.16'17 Of the
20 patients studied, a delay of 26 msec was documented
in the eye of a patient having unilateral idiopathic cen-
tral serous choroidopathy with normal visual acuity.
Because this patient demonstrated the largest VEP de-
From the Schnurmacher Institute for Vision Research, State Uni-
versity of New York,* State College of Optometry, New York, New
York, and New York University Medical Center, f
Submitted for publication: November 17, 1984.
Reprint requests: Jerome Sherman, OD, SUNY State College of
Optometry, 100 East 24th Street, New York, NY 10010.
lay of all our maculopathy patients and because VEP
delays in central serous choroidopathy had never pre-
viously been reported, we decided to limit this current
study to central serous choroidopathy patients. This
disease entity was an ideal one to study because (a) it
is often a reversible, limited condition which resolves
with or without treatment; (b) there is usually a normal
control eye; (c) the typical time course of its resolution
is favorable for detailed investigation.
There have recently been two additional reports 1819
following ours16 in which VEP delays have also been
documented in patients with central serous choroi-
dopathy. In this current study, we performed VEPs on
a series of ten patients who were diagnosed as having
unilateral idiopathic central serous choroidopathy. We
followed seven of these patients until the condition ei-
ther fully resolved (six patients) or partially resolved
(one patient). Unlike previous reports, we will dem-
onstrate that as the condition resolves, the VEP returns
to normal and becomes nearly superimposable with
the VEP from the unaffected eye.
Materials and Methods
We evaluated ten consecutive patients (ranging in
age from 27 to 49 yr, with a mean age of 38.8 yr) di-
agnosed as having active central serous choroidopathy
in one eye (Table 1). All patients had the typical
ophthalmoscopic and fluorescein angiographic finding
of serous detachment of the neurosensory retina in the
macula. Each patient had normal pupillary responses
and normal-looking optic discs. The ocular examina-
tion was otherwise normal except for serous detach-
ments of the retinal pigment epithelium (RPE) outside

214

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 No. 2 VEP DELAYS IN CENTRAL SEROUS CHOROIDOPATHY / Sherman er ol.
the macula in the fellow eye in two patients (patient
6, patient 8) and one patient with bilateral keratoconus
(patient 4). Visual acuities ranged from 20/20 to 20/
70 in the affected eye during the active phase. Informed
content was obtained from each patient prior to un-
dertaking the study.
Pattern-reversal VEPs were recorded from each eye
separately, using an averager (Nicolet CA-1000) and
visual stimulator (Nicolet 1005, Madison, WI). A gold
cup electrode (Grass; Quincy, MA), attached to the
scalp 2 cm above the inion, was used to record the
VEP. Two ear clip electrodes were used, one for the
reference and the other for the common ground. Elec-
trode impedance was maintained below 6000 Kohms.
An artifact rejection was utilized to reject any signal
greater than about 50 nV which might be created by
blinks or large eye movements. Pattern elements con-
sisted of squares of 14, 28, and 56 min of arc presented
in a checkerboard pattern. The pattern elements were
measured by their edge and not diagonally. The pattern
was reversed at 7.5 reversals/sec. The stimulus distance
was 1 meter. The overall field size at 1 m was 12°
vertical by 15° horizontal. Mean luminance was main-
tained at 25 cd/m 2 and contrast (L max - L min)/(L
max + L min) at 76%. The patients were optically cor-
rected for the stimulus distance and mydriatics and
cycloplegics were not utilized. The analysis time was
set at 200 msec, and between 100 and 200 responses
were averaged for each trial.
VEP amplitudes on all patients were determined by
measuring the difference between the major positive
and major negative peaks. Peak times (to be referred
to as "latency") were taken from the stimulus trigger
to the highest positive peak. We have elected not to
use the standard nomenclature of P100, P135 etc be-
cause the standard reversal rate of 1 HZ (2 reversals/
sec) was not utilized (see above). In addition to mea-
suring monocular latency and amplitude, interocular
latency and amplitude differences were calculated. The
absolute value of these interocular differences were
compared to a control group consisting of 16 normals,
evaluated as part of a previous study performed by
these authors 17 (Table 2). If an interocular difference
(either amplitude or latency) of a patient was greater
than 2.5 standard deviations from the mean interocular
difference of the control group, we considered the dif-
ference to be statistically significant.
Results
The results of the VEPs in the active stage and re-
solved stage in these ten cases are listed in Table 1.
Three patients were lost to follow-up.
The mean latency in the normal unaffected eyes was
116 ± 5.1 msec to 14-min squares, 109.8 ± 6.7 msec
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215
to 28-min squares, and 108.8 ± 6.7 msec to 56-min
squares. The mean latency of the central serous eyes
(during the active phase) was 136.8 ± 11.8 msec to 14-
min squares, 126.5 ± 15.4 msec to 28-min squares,
and 120.9 ± 10.5 msec to 56-min squares (Table 3).
The central serous eye compared to the normal eye
demonstrated a mean VEP delay of 21 ± 10.3 msec to
14-min squares, 16.7 ± 9.2 msec to 28-min squares,
and 10.6 ± 6.0 msec to 56-min squares (Table 4).
Individually, 7 of the 8 patients (88%) giving record-
able responses to 14-min squares demonstrated statis-
tically significant interocular VEP delays. All 10 pa-
tients gave recordable responses to 28-min squares, and
7 of these (70%) demonstrated statistically significant
interocular VEP delays. Nine patients gave recordable
responses to 56-min squares, and of these 9, 5 (56%)
demonstrated statistically significant interocular VEP
delays. When considering all 3 square sizes, 9 out of
10 patients (90%) had significant interocular delays in
the affected eye.
When analyzing the data for effects on amplitude,
we found that only 13% of the patients (1 out of 8)
demonstrated statistically significant interocular re-
ductions in amplitude to 14-min squares, 20% (2 out
of 10) to 28-min squares, and 22% (2 out of 9) to 56-
min squares. Overall, 30% of patients demonstrated a
significant decrease in amplitude when considering all
three square sizes.
Case Reports
Three exemplary cases are presented here with find-
ings confirming the diagnosis of idiopathic central se-
rous choroidopathy and VEPs performed during the
active phase and repeated after the condition resolved.
Case 1 was treated with laser 2 wk after the diagnosis
was established. Case 2 was followed for 6 months
without spontaneous resolution of the fluid and then
treated with laser. Case 3 fully resolved spontaneously
within 7 months.
Case 1. Patient 6, a 39-yr-old white policeman, presented
with a complaint of a "dark spot" in his vision in the left eye
for the past 6 months. Best corrected visual acuities were 20/
20 in the right eye and 20/30 in the left eye. Ophthalmoscopy
revealed a large area of fluid in the macula of the left eye and
RPE changes in the macula of the right eye. On Amsler grid,
the neurosensory retina infero-temporal to the fovea (Fig. 1).
VEPs recorded from the left eye demonstrated significant
interocular delays to all 3 square sizes with a 43 msec delay
to 14-min squares (the largest delay recorded from any patient
in our study), Figure 2A, a 12 msec delay to 28-min squares,
and a 16-msec delay to 56-min squares. The interocular am-
plitude differences were not statistically significant. Because
the condition had failed to resolve spontaneously, the patient
was eager to undergo laser photocoagulation, which was per-
formed by a local ophthalmologist. Three weeks after treat-
ment, the patient returned to us. The initial symptoms had
 216 INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / February 1986 Vol. 27

Table 1. Patient data summary

VEPs during active
fiV/msec
Photostress Amsler Square
Patient Age/Sex Visual acuity recovery (sec) Gridf Sizes\\ OD. OS

1 40/M OD: 20/20"2* 300 + 14' 8.8/154 15.0/128

OS: 20/20+3 24 28' 6.8/135 10.2/121
2 27/M OD: 20/60* 300 + 14' 3.3/144 6.0/118
OS: 20/20 20 28' 2.3/137 5.9/108
3 49/F OD: 20/20 NM§ 14' 7.6/112 8.4/131
OS: 20/25+1* NM + 28' 9.2/112 10.5/120
4 34/M OD: 20/70* 15 + 14' Not Recordable,
OS: 20/25 18 28' 3.1/138 4.1/108
5 38/M OD: 20/20"3 60 14' 7.5/120 7.7/138
OS: 20/30-2* 25 min + 28' 6.1/105 4.3/124
6 39/M OD: 20/20 40 14' 6.9/111 4.7/154
OS: 20/30* 300 + 28' 5.4/114 4.5/126
7 49/M OD: 20/40* NM + 14' 6.8/120 18.0/112
OS: 20/20 NM + 28' 7.2/126 13.5/106

8 40/M OD: 20/20 60 14' 3.2/116 1.9/129

OS: 20/30* 90 + 28' 5.0/120 3.7/127
9 38/M OD: 20/50* NM + 14' 6.5/135 9.0/116
OS: 20/20 NM + 28' 2.4/137 13.2/108

10 29/M OD: 20/40* 90 14' Not Recordable,

OS: 20/15 40 28' 2.6/100 4.9/98

• The affected eye. § NM = not measured

t + = metamorphopsia; - = normal || VEPs to 56-min squares are not included in table.
JNA == not applicable

plitude differences were not statistically significant. Because
the condition had failed to resolve spontaneously, the patient
was eager to undergo laser photocoagulation, which was per-
formed by a local ophthalmologist. Three weeks after treat-
ment, the patient returned to us. The initial symptoms had
disappeared, but the patient was now aware of a scotoma.
Visual acuity was still 20/30 in the treated eye. On Amsler
grid viewing, metamorphopsia was not present, but a 6° sco-
toma was reported about 2° away from fixation. The scotoma
corresponded to a photocoagulation burn temporal to the
fovea, but no fluid was observed. VEPs recorded after treat-
ment did not demonstrate any interocular delays from the
previously affected eye, and the responses from each eye were
nearly superimposable (Fig. 2B).
Case 2. Patient 5, a 38-yr-old white postal worker presented
with complaints of a "blurry spot" in the center of his field
of vision in the left eye of approximately 1 month's duration.
Entering visual acuities were 20/20 in the right eye and 20/
30"' in the left eye. Ophthalmoscopy of the left eye revealed
edema residues in the left macula with paramacular edema.
The right eye was unremarkable. On viewing the Amsler grid,
the patient reported a 7° circular area of metamorphopsia
around the fixation point in the left eye. Viewing with the
right eye did not reveal any abnormalities. Macular dazzle
recovery time was 1 min in the right eye to read 20/25 and
25 min in the left eye to read 20/40. Fluorescein angiography
revealed a serous detachment of the neurosensory retina su-
pero-nasal to the fovea in the left eye (Fig. 3). VEPs were
recorded and interocular delays were evident to all three
square sizes (Fig. 4A), with an 18-msec delay from the affected
eye to 14-min squares, a 19-msec delay to 28-min squares,
and a 20-msec delay to 56-min squares. The interocular am-
plitude differences were not statistically significant. The pa-
tient was followed monthly for the next 5 months during
which time there was no change in acuity, symptoms,
ophthalmoscopic appearance, or VEP latency. After the sixth
month of follow-up, fluorescein angiography was repeated.
Since the fluid failed to resorb and leakage was still evident,
the patient decided to have laser photocoagulation performed.
Three weeks after treatment, the patient's subjective symp-
toms disappeared and visual acuity improved in the affected
eye to 20/20. Ophthalmoscopy revealed some RPE defects
nasal to the fovea, but fluid was no longer evident. On Amsler
grid, the patient did not report any metamorphopsia in either
eye. Photostress recovery times were 15 sec in the right eye
and 35 sec in the left eye. VEPs recorded from the left eye
were now normal, did not exhibit any delays compared
with the right eye and were practically superimposable
(Figure 4B).
Case 3. Patient 1, a 40-yr-old white male, presented with
complaints of seeing a film over the right eye and a "halo"
in the center of his vision. Visual acuities were 20/20 through
the right eye and 20/20 through the left eye. Examination of
the right eye through a Goldmann 3-mirror lens revealed
edema of the central 7° of the retina. The central retina of
the left eye was within normal limits. Drusenlike changes
were evident throughout the posterior poles of both eyes.
Testing with the Amsler grid revealed an approximately 7°
central, round relative scotoma when viewed through the
right eye. No visual field abnormalities were evident when
viewing the Amsler grid through the left eye. Results of mac-
ular dazzle revealed recovery times of 300 sec in the right
eye to achieve a visual acuity of 20/50 and 24 sec in the left
eye to achieve 20/20. Fluorescein angiography revealed a se-
rous detachment of the neurosensory retina supero-nasal to
the macula in the right eye (Fig. 5). VEPs were recorded to

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 No. 2 VEP DELAYS IN CENTRAL SEROUS CHOROIDOPATHY / Sherman er ol. 217

Table 1. (cont'd)
VEPs after condition resolved n V/msec
phase
Square
Delay sizes O.D. OS. Delay Notes and comments

26 msec 14' 13.5/136 13.7/135 1 msec Resolved without treatment VA = 20/15,

14 msec 28' 10.5/131 9.4/134 none OD O.D.
26 msec 14' NAft NA NA Lost to follow-up.
29 msec 28' NA NA NA
19 msec 14' NA NA NA Lost to follow-up.
8 msec 28' NA NA NA
OD 14' Not Recordable, OD Resolved without treatment; VA
30 msec 28' 5.6/102 7.0/101 1 msec = 20/30 O.D., corneal striae, O.U.
18 msec 14' 8.9/111 11.6/111 0 msec Resolved after photocoagulation; VA
19 msec 28' 10.3/104 9.1/106 2 msec = 20/20, O.S.
43 msec 14' 8.0/109 6.5/113 4 msec Resolved after photocoagulation; VA
12 msec 28' 5.0/110 4.3/117 7 msec = 20/30, O.S.
8 msec 14' 4.8/125 10.4/117 8 msec Partially resolved after photocoagulation,
20 msec 28' 9.5/119 17.9/108 11 msec VA = 20/20, O.D.
Serous RPE detachment outside the
macula O.S.
13 msec 14' 1.7/124 3.9/113 none OS Resolved without treatment; VA = 20/25,
7 msec 28' 5.0/106 2.2/110 4 msec O.S.
19 msec 14' 9.0/119 11.2/114 5 msec Resolved without treatment; VA = 20/25,
29 msec 28' 9.4/119 11.9/111 8 msec O.D. Serous RPE detachment outside
the macula O.S.
OD 14' NA NA NA Lost to follow-up.
2 msec 28' NA NA NA Only patient not showing delays.

pattern stimuli during this initial visit. Interocular VEP la-
tencies from the right eye to 14,28, and 56 min of arc squares
were significantly delayed. Although the first positive peak is
somewhat broadened and not well formed from the right eye
to 14-min squares (Fig. 6A), an interocular delay of 26 msec
from the right eye was estimated as was a 14-msec delay to
both 28- and 56-min squares.
The interocular amplitude differences were not statistically
significant. The patient was reexamined 7 months later. At
that time, the previous presenting symptoms had subsided,
and visual acuities were right eye, 20/15"' and left eye, 20/
15. Ophthalmoscopy revealed some drusen-like deposits or
edema residues throughout the posterior poles of both eyes,
but no notable macular changes. Macular dazzle was 20 sec

Table 2. Mean values for VEP Latency, amplitude and latency, amplitude difference between eyes
of 16 normal controls (32 normal eyes)
Mean difference Mean difference
Mean latency Mean amplitude in latency in amplitude
Square size (msec) (msec)

14 minute 119.2 ±8.4 9.8 ± 3.9 2.9 ±3.1 1.9 ±2.0

28 minute 113.4 ±7.6 9.8 ± 3.7 3.7 ± 2.6 1.6 ± 1.1
56 minute 110.6 ±7.2 8.9 ± 3.2 3.8 ± 4.3 2.1 ± 1.4

Table 3. Mean values for VEP latency and amplitude for the unaffected eye and for the affected eye
often central serous choroidopathy patients
Unaffected eyes Affected eyes

Mean latency Mean amplitude Mean latency Mean amplitude

Square size (msec) (msec)

14 min 116.0 ±5.1 8.7 ±4.9 136.8 ± 11.8 5.5 ±2.4

28 min 109.8 ± 6.7 7.8 ±3.3 126.5 ± 10.4 4.8 ±2.5
56 min 108.8 ±6.7 8.5 ±3.0 120.9 ± 10.5 5.7 ±2.7

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 218 INVESTIGATIVE OPHTHALMOLOGY 6 VISUAL SCIENCE / February 1986 Vol. 27

Table 4. Mean values for interocular latency and treatment with laser photocoagulation is employed if
amplitude differences in central serous resolution does not occur spontaneously within 4-6
choroidopathy patients months. To our knowledge, when we first reported sig-
nificant interocular VEP delays in a patient having
Mean latency Mean amplitude
difference difference unilateral, idiopathic central serous choroidopathy as
Square size (msec) part of a larger study on maculopathy patients,16 there
had been no previous reports of VEP delays occurring
14 min 21.0 ± 10.3 3.2 ± 3.6
28 min 16.7 ± 9.2 3.0 ± 3.2 in this condition. More recently, however, Papakos-
56 min 10.6 ± 6.0 2.9 ± 3.9 topoulos, et al18 have reported mean interocular VEP
delays of 7.3 msec in 6 patients having unilateral, cen-
tral serous choroidopathy and Han, et al19 presented
evidence of VEP delays in 18 patients having this con-
in the right eye and 10 sec in the left eye. No abnormalities
were reported when viewing the Amsler grid. VEPs revealed
dition. Unlike these two reports, in the present study
negligible differences in the peak times of the responses from we demonstrated that as the unilateral condition re-
the right and left eyes (Fig. 6B). solves, the VEP returns to normal and becomes nearly
superimposable with the VEP from the unaffected eye.
The mechanism(s) responsible for VEP delays in
Discussion central serous choroidopathy is unknown. The fluid
Idiopathic central serous choroidopathy, a clinical may cause receptor tilt resulting in an abnormal Stiles-
entity primarily seen in young males, is characterized Crawford Effect which decreases the efficiency of light
by a flat, serous detachment of the sensory retina of energy,21 Figure 7 demonstrates that a series of neutral
the posterior pole and is usually a benign, self-limiting density filters progressively delays the VEP from a nor-
condition which resolves spontaneously. Generally, mal eye while causing only minimal reduction in am-

Fig. 1. Fluorescein an-

;iography of the left eye re-
pealed an area of leakage in-
ero-temporal to the fovea;
eft, early phase, right, late
)hase.

Fig. 2. Left, VEPs recorded

A.
during the active phase; 43-
2/24/84 3/26/84 msec interocular delay, O.S.,
VA: 00 = 20/20 VA: 00=20/20
OS=20/30
demonstrated. Right, VEPs
OS-20/30
recorded once condition fully
, OD pllsS.BSuv
resolved; 4-msec interocular
delay, O.S., demonstrated;
responses are nearly super-
p!t*4.7uv imposable. (In this and in
the following VEP traces, ptt
VEPs in resolved stage
= peak to trough amplitude
VEPs during active phase (patient was treated)
and positive is up.)

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 No. 2 VEP DELAYS IN CENTRAL SEROUS CHOROIDOPATHY / Sherman er al. 219

Fig. 3. Fluorescein angiography of

the left eye revealed a large area of
leakage supero-nasal to thefovea.A
second area, temporal to the fovea,
did not increase in size from the early
to the late phase; left, early phase,
right, late phase.

1/12/B4
Fig. 4. Left. VEPs recorded 6/13/83
VA. 00=20/20
during the active phase; 18- VA: O0-20/20" 3 OS*20/20
OS-20/30" 2
msec interocular delay, O.S.,
demonstrated. Right, VEPs
recorded once condition fully
resolved; no interocular delay
evident from the left eye; re-
sponses are superimposable.
VEPs during active phase VEPs in resolved stage
(patient was treated)

plitude. Since a 2.0-log unit filter can result in a 40-
50-msec delay, the VEP delays reported here in central
serous can be fully explained as a mere passive effect
due to less light reaching the outer segments of the
photoreceptors.
Another possible mechanism is that the fluid impairs
the integrity of the neuronal membranes, thus inter-
fering with dynamics of neurotransmitter action in-
volved in the intraretinal feedback loop modulating
adaptational processes. The best neurotransmitter
candidate for such modulatory activity is dopa-
mine, 2223 which has recently been found in the human
retina.24 VEP delays in dopaminergic deficiency due
to Parkinson's disease (PD) have been demonstrated
by Bodis-Wollner and Yahr,5 who proposed a retinal
origin of the delays.

Fig. 5. Fluorescein an-

giography revealed a small
area of leakage supero-nasal
to the macula in therighteye;
Left, early phase. Right,, late
phase.

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 220 INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE / February 1986 Vol. 27

7/13/81 3/15/82
VA: OD=20/20 VA: 00=20/15" '
AO-Oft/Ort•3
Fig. 6. Left, VEPs recorded
OS-20/15 during the active phase; a 26-
.1 54msec .136msec
msec interocular delay, O.D.,
f\A
00 / ~ \
—\ /—"^\
14' ' 0 0 '-s. demonstrated. Right, VEPs
1 A* \\
os 121m \/^128msec
OS ^\ ^^
„ recorded once condition fully
resolved; a I-msec interocu-
\ / \ lar delay observed, O.D.; re-
\ /\ / \ , ptt.15.0uv \ i' _ ' sponses are nearly superim-
/ V ^ \ / 135msec posable.

VEPs during active phase VEPs in resolved stage

(resolved spontaneously)

More recently, Kupersmith et al,6 in addition to
finding VEP delays in a group of PD patients, recorded
oscillatory potential electroretinograms in the same
group. These potentials are believed to reflect activity
in the inner nuclear layer and are probably mediated
by the amacrine cells,25 or the interplexiform cells.26
Since both cell types contain dopamine 27 ' 28 and since
the application of dopamine to the retina in vitro alters
the oscillatory potential,29 one might expect abnormal
oscillatory potentials in PD. However, Kupersmith et
al6 report normal oscillatory potentials in the same
group of patients with PD who demonstrated. VEP de-
lays. Although these results do not support the conten-
tion that a dopamine deficiency exists at the retinal
level in PD, they cannot preclude the retina as a possible
site of dysfunction in PD. 6
One may argue that since the VEP is normally a
macular-dominated response, any macular lesion, such
as CSR, may uncover a paramacular potential which
normally has a greater latency.30 In normal patients,
28' square size
ptt=12.96uv
NDF 0 dysfunction. If VEPs to squares are delayed, macular
NDF 1.6
ptt=16.23uv
NDF 2.0
ptt=13.68uv
NDF 2.6
ptt=10.66uv
j I
Fig. 7. When less light reaches the photoreceptors as a result of
the interposition of a series of neutral density filters (NDF), the VEP
becomes progressively delayed.
this paramacular potential is often hidden in the earlier
and larger macular potential. However, upon careful
inspection of the VEP wave-forms from the nine CSR
patients with delays reported in this study, one observes
that the positive and negative waves appear to be de-
layed in the affected eye when compared with the un-
affected eye, rather than the absence or reduction of
just the major positive peak.
Wildberger31 has shown that stimulation of the lower
half of the retina results in VEPs which are approxi-
mately 20 msec later than those resulting from stim-
ulation of the upper half of the retina. This suggests
that a lesion affecting only the upper half of the macula
may result in a delayed VEP. In the nine patients with
CSR with delays reported in this study, three had le-
sions primarily inferior to the fovea, three had lesions
primarily superior to the fovea, and three had relatively
central lesions. No correlation exists between the lo-
cation of the detachment and the latency delay.
Although the explanation of VEP delays in central
serous choroidopathy will be the subject of ongoing
study, the presence of these delays has been well dem-
onstrated in this preliminary study and in other reports
as well. A delayed VEP to squares of various spatial
frequencies can therefore no longer be used in the dif-
ferential diagnosis of CSR vs demyelinating optic nerve
disease, especially central serous choroidopathy, must
be ruled out before diagnosing a visual pathway dys-
function. This point is not trivial since Kraushar 32 has
reported three patients diagnosed by ophthalmologists
as having multiple sclerosis who actually had recur-
rences of central serous choroidopathy, which was
proven angiographically. Since both central serous
choroidopathy and multiple sclerosis produce episodes
of monocular visual loss in young adults, misdiagnosis
is possible especially in those cases with only minimal
fluid accumulation. In such questionable cases, the cli-
nician should simply rely upon the results of the
swinging flashlight test, macular dazzle, color vision,
and fluorescein angiography, but certainly not the VEP.

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 No. 2 VEP DELAYS IN CENTRAL SEROUS CHOROIDOPATHY / Sherman er ol.
Although we have demonstrated that VEPs to
squares are not useful alone for differential diagnosis,
VEPs to gratings might be since VEP delays to gratings
of some orientations but not to others have been re-
ported in multiple sclerosis33 but not in macular dis-
ease. It remains to be demonstrated whether such VEP
orientation asymmetries will permit the differential di-
agnosis of macular vs optic nerve dysfunction to be
made with any certainty.
Finally, the general guideline sometimes espoused
by clinicians that VEPs are delayed in optic nerve dis-
ease but reduced in amplitude in retinal disease should
be abandoned. Not only do delays as great as 43 msec
occur in retinal disease (Case 1), but many cases of
non-demyelinating optic neuropathes have no (or only
slight) VEP delays.34'35 Reductions in amplitude, both
in retinal disease and optic neuropathes, grossly cor-
relate with the visual acuity reduction.31
Key words: central serous choroidopathy, visual evoked po-
tential delays, macular disease, optic nerve disease
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