Yonago Acta medica 2003;46:65–75

Slow and Fast Oscillation Electrooculography in Central
Retinal Vein Occlusion: A Comparison between Affected
Eyes and Fellow Intact Eyes
Machiko Inoue, Akihiko Tamai*, Shiro Hatta† and Yuji Sasaki†
Clinic of Ophthalmology, Hamada National Hospital, Hamada 697-8511, *Clinic of Ophthalmology, Hino Hospital Association Hino Hospital, Tottori 689-4504 and †Division of Ophthalmology and Visual Science, Department of Medicine of Sensory and Motor Organs, School of
Medicine, Tottori University Faculty of Medicine, Yonago 683-8504 Japan
Using an automated electrooculograph, the Nidek EOG-2, slow and fast oscillations (SOand FO) of an electrooculogram (EOG) were recorded in 21 patients with unilateral,
ischemic central retinal vein occlusion (CRVO). Patient age ranged from 49 to 81 years(average: 68 years of age). Fellow eyes in all patients were intact, and served as controls.
Results showed that the L/DSO (the light peak/dark trough ratio of the SO), the RfFO [theaverage ratio in percentage of the maximum amplitude in the dark period (AD)/the minimum amplitude in the light period (AL) during FO measurement], the dfFO (the average
difference in µV between AD and AL), and the df/mFO [the percentage ratio of the dfFO to
the average amplitude of AD + AL (m)] were significantly decreased in the affected eyescompared with the fellow eyes. These results suggest that with regard to SO and FO
origin and occurrence, the outer layer of the retina, especially the basal membrane of theretinal pigment epithelium or the choroid may be involved in the etiology of CRVO. Thesefindings correlate with the grade of microcirculatory disturbance or ischemia in the inner
layer of the retina. Furthermore, a statistically significant difference was detected in thecorrelation between each FO parameter and corrected visual acuity at the time of
examination of the affected eyes. There was no significance between the SO parameterand the visual acuity. Therefore, it might be possible to presume that the FO parameters
can be used as indicators for detecting the severity of macular functional disturbance andpredicting the visual outcome for this entity.
Key words: central retinal vein occlusion; electrooculogram; fast oscillation; retinal pigment epithelium; slow oscillation

Central retinal vein occlusion (CRVO) results froma thrombotic occlusion, most commonly due toarteriosclerosis-related thrombus at the level of thelamina cribrosa. CRVO provides 2 forms of clinicalpresentation, that is, a mild form of non-ischemic
CRVO (also known as partial, incomplete, hyper-

Abbreviations: AD, maximum amplitude in the dark period; AL, minimum amplitude in the light period during FO
measurement; BRVO, branch retinal vein occlusion; CRAO, central retinal arterial occlusion; CRVO, central retinal
vein occlusion; dfFO, average difference in µV between AD and AL during the FO measurement; df/mFO, percentage
ratio of the dfFO to the average amplitude of AD + AL (m); EOG, electrooculogram; ERG, electroretinogram; FO, fast
oscillation; L/DSO, light peak/dark trough ratio of the SO; RfFO, average ratio in percentage of AD/AL; SO, slow
oscillation

65

M. Inoue et al.

permeable or venostatic retinopathy), and a severe
form of ischemic CRVO (complete or hemorrhagic
CRVO) (Hayreh, 1983; Ohba, 2002).
Clinical and experimental evidence indicatesthat non-ischemic CRVO is caused by a mild occlusion of the central retinal vein, but that ischemic
CRVO is caused by a severe or complete occlusionof the central retinal vein associated with retinal
ischemia or significant hypoxia (Hayreh et al.,1989). In a histopathologic study, Green and others(1981) found that 13.8% of CRVO patients wereassociated with central retinal arterial occlusion(CRAO), and 10.8% with branch retinal artery occlusion. Although the central retinal artery supplies
blood only to the inner retinal layers, simultaneous
occlusion of the central retinal vein and artery results in damage to all layers of the retina, including
the retinal pigment epithelium.
The electroretinogram (ERG) is reported to be
helpful in predicting a visual prognosis in CRVO
because its response is sensitive to retinal ischemia(Henkes, 1953; Sabates et al., 1983; Sakane et al.,
1989; Ohn et al., 1991) which may be one of theimportant factors for visual outcome. The ordinary
slow oscillation (SO) of the electrooculogram(EOG) on the other hand reflects the function of theretinal pigment epithelium and photoreceptor complex, and appears to be unrelated to the neural network whose function is controlled mainly by retinal
circulation. However, it is well established that theEOG becomes very abnormal in CRAO, the severest form of retinal ischemia, and therefore the EOG
appears to be indirectly related to or governed byretinal circulation (Thaler and Heilig, 1977).
Branch retinal vein occlusion (BRVO) does
not give proof of any abnormalities on the ERG or
EOG unless the lesion is sufficiently large, because
the ERG and EOG reflect the mass activity of theretina (Karpe and Uchermann, 1955; Arden et al.,
1962; Hara and Nagatomo, 1995). On the contrary,
in his original description of the EOG, Arden
described a patient with CRVO whose EOG wasseverely deteriorated (Arden et al, 1962). Carr andSiegel (1964) found abnormal EOGs in CRVO
where the ERG remained relatively normal.
Ashworth (1966) reported 4 patients with CRVO,

all of whom had deteriorated EOGs in varying
degrees. Papakostopoulos and others (1992) reported that the light peak/dark trough ratio of the
SO (L/DSO) of the EOG (Arden et al., 1962) was
significantly reduced in the affected eyes of a groupof patients with CRVO compared with the unaffected fellow eyes.
The fast oscillation (FO) of the EOG, which is
the rapid initial deflection of opposite polarity occurring at the initial stage of the light and dark periods in the EOG procedure (Kolder and Brecher,1966) also showed abnormal FO patterns in patientswith ischemic retinopathy or CRAO (Thaler et al.
1977; Tamai et al., 1997).
Our previous study in patients with BRVO or
CRVO (Tamai et al., 1997) suggests that analysis of
the SO and FO of the EOG may provide information regarding the dysfunction of the stratiform
layer in the affected retina (Hara et al., 1991) andchoroid.
In the present study, the SO and FO variables
are compared with those of the contralateral intact
eyes in patients with unilateral, ischemic CRVO,
with special emphasis on the corrected visual acuityat the time of EOG examination of the affectedeyes.

Patients and Methods

Patient selection
Twenty-one patients (12 men, 9 women; age range
49–81 years, mean 68 years) with unilateral, ischemic CRVO were randomly chosen for EOG recording over the past 4 years (August 1996 to September
2000) at the Department of Ophthalmology, Tottori
University Hospital (Table 1). Under the ophthalmoscope, it was revealed that their fundi in the affected side showed a flame-shaped bleeding in thewhole retina and a remarkable papilloedema, associated with dilated and tortuous retinal veins andlots of cotton-wool patches. Fluorescein angiography revealed evidence of extensive retinal capillary non-perfusion in their fundi. Duration fromonset estimated to be 5 to 167 days averaging 30.9
66

EOG slow and fast oscillations in CRVO

Table 1. Clinical data of 21 patients with unilateral, ischemic CRVO at the time of EOG examination
Patient
numberAge (year)

Sex

Affected eye

1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21

74
68
54
71
66
73
68
60
71
81
78
72
49
63
70
59
71
81
74
68
58

FemaleMale
FemaleMale
Male
FemaleFemaleMale
Male
FemaleFemale
Male
Male
Male
FemaleMale
Male
FemaleFemale
Male
Male

Right
Left
Left
Left
Left
Right
Left
Right
Right
Left
Right
Right
Right
Left
Left
Right
Left
Right
Left
Right
Left

Duration from Corrected
onset (day)visual acuity
34
26
11
58
5
8
39
10
21
14
123
13
32
12
167
8
17
6
15
16
14

0.1
0.1
1.2
0.01
0.1
0.7
0.2
0.3
0.02
CF*
0.5
0.02
0.04
0.4
0.01
0.01
0.06
0.04
0.01
0.1
0.5

General complication
Hypertension
Hypertension

Hypertension
Hypertension
Hypertension

Hypertension

Hypertension
Hypertension

Hypertension*CF, counting figers: estimated to be 0.001.

days at the time of EOG examination. Nine out of
the 21 patients had hypertension as a general complication (Table 1). Fellow eyes in all patients were
ophthalmoscopically and fluorescein-angiographically intact, and served as controls.
Patients were excluded from this study if they
had an opaque media, a bilateral refractive error
difference of more than 3 diopters, diabetes mellitus
or a history of ocular surgery, photocoagulation,
anticoagulant therapy or fibrolytic therapy.

background luminance of 1,270 lux, when measured at the location of the patient’s eyes.
For every patient, cup-shaped silver-silver
chloride conductive electrodes, 8 mm in diameter,
were placed beside both canthi of each eye on theorbital margin, and a grounding electrode, with thesame cup shape, was placed on the left earlobe, asroutinely used. Before setting these electrodes, theskin was cleaned with 90% alcohol, and then electrodes were applied with a conductive paste. Electrode resistance was below 10 kΩ.
Before SO recording, a 10-min adaptation
period at a background luminance level of 1,270 lux
was given to the patients. Then the patients were
instructed to fixate alternately on a pair of targets on
the screen inside the dome. The 2 targets substended 40˚ to the eye, and were presented alternately with a frequency of 0.5 Hz.
On the SO recording, where 20 min of darkness was followed by 20 min of illumination, EOG
measurements were started 40 s before the end of

SO and FO recordings
Using a newly devised automated electrooculograph, the Nidek EOG-2 (Nidek, Gamagori, Japan)(Nakao et al., 1995), the SO and FO were recordedin each patient. The EOG-2 consists of a dome, apersonal computer, an index controller, an amplifier, a printer and an EOG pen recorder. Inside thedome is a hemispheric screen with a radius of 300
nm. Four tungsten lamps (115 V, 50 W) produce a67

M. Inoue et al.

AD1

AD2

AL1

RfFO

AD3

AL 2

AD
AD
+
+
(
AL
AL
=
1

2

1

2

AD4

AL 3

•••+

n

dfFO =

df/mFO =

ADn
AL n

AD5

AL 4

AL 5

) × 100 (%)(AD1 – AL1) + (AD2 – AL 2) + • • • + (ADn – AL n)n

dfFO(AD1 + AL1 + AD2 + AL 2 + • • • + ADn + AL n) / 2n(µV)

Fig. 1. Fast oscillation (FO) parameters, the RfFO, the dfFO and the
df/mFO, calculated in this survey.
AD, maximum amplitude during
the dark period; AL, minimum amplitude in the light period during
FO measurement; n, number ofcycles (dark-light period of 1 mineach), 10 cycles in total.

× 100 (%)

(10 ≥ n ≥ 3)each 1-min period during the dark and light adaptations. Six out of 10 EOG amplitudes were automatically averaged and recorded every 1 min throughthe EOG artifact rejection system on the Nidek
EOG-2. Twenty out of the 21 patients gave reliabledata on the test.
The SO shows a trough in the dark adaptation(dark trough) and a peak in the light adaptation(light peak) in response to dark and light periods ofapproximately 12.5 min each. The L/DSO developed by Arden and others (1962) was automaticallycalculated as an SO parameter in the present survey.
Then the FO was recorded in all patients.
Before the FO recording, the patients were subjected to a 10-min pre-light adaptation in the same manner as in the SO recording. The 2 targets subtended
40˚ to the eye, and were presented alternately with afrequency of 0.5 Hz. The dome was periodically
illuminated for 1 min followed by 1 min of darkness. The measurements were started 40 s after
each dark or light period began. There were 10
measurements in each dark or light period as in the
SO recording. The mean of the 6 EOG amplitudes
recorded at the end of each dark or light period was
automatically calculated.
In this study, the calibration sensitivity for the
pen recorder was 200 µV/division on the printer.

The time constant of the amplifier was set at 3 s, anda high frequency cutoff of –3 dB was set at 20 Hz
for both SO and FO recordings.
Pupillary dilation provides better control ofretinal illumination levels, but prolongs the time for
the EOG examination and may make the examination somewhat more uncomfortable for some patients. Therefore, the SO and FO recordings were
performed with pupils undilated.
The FO parameters were calculated referringto the report by De Rouck and Kayembe (1981).
Namely, the RfFO, which is the average ratio inpercentage of the maximum amplitude in the dark
period (AD)/the minimum amplitude in the lightperiod (AL), and the dfFO, which is the average
difference in µV between AD and AL during the FO
measurement, were calculated in addition to a newly designed df/mFO, which is the percentage ratio ofthe dfFO to the average amplitude of AD + AL (m),only if at least 3 successive steps showed some
identical amplitude change (Fig. 1). Dated andoccasional large amplitude changes were not taken
into account. In the df/mFO, the influence of fluctuation of the base value to the FO pattern is supposed
to be minimized compared to the dfFO (Nakao et al.,
1995; Tamai et al., 1997).

68

EOG slow and fast oscillations in CRVO
(µV)

(µV)

SO

1200

EOG amplitude

EOG amplitude

1000
800
600
400

FO

1000

R
L

R
L

800
600
400
200

200
0

D
0

0

L

10

20

30

40
(min)

Time

DL
0

5

10

15

Time

20
(min)

Fig. 2. EOG slow oscillation (SO) and fast oscillation (FO) patterns in both eyes of Patient 8 (60-year-old male,ischemic CRVO patient). R, right eye (affected side); L, left eye (fellow intact side). D, dark period; L, light period(horizontal axis).

All values were expressed as mean ± SD.
Statistical analysis was performed with MannWhitney’s U test. Spearman’s rank coefficient ofcorrelation test was applied for correlation analysis.
A P value of < 0.05 was considered statisticallysignificant.

Affected eye

3.0

Results
Practical EOG SO and FO patterns in both eyes ofPatient 8 (a 60-year-old male patient with unilateral, ischemic CRVO) are demonstrated in Fig. 2.
In this patient, reduced or deteriorated SO and FO
patterns were observed in his affected eye (righteye), although his fellow intact eye (left eye) showed normal patterns in bothrecordings.
Mean ± SD (n = 20)

Fellow intact eye

1.38 ± 0.37
1.93 ± 0.33
*P < 0.01

2.5*

Figure 3 shows the distribution of the L/DSO in
20 affected and fellow intact eyes of 20 patientswith ischemic CRVO excluding 1 patient (Patient10), whose data were unreliable. Nineteen out of

2.0

L/DSO

L/DSO

1.5

1.0

0.5

0
1

2

3

4

5

6

7

8

9

10

11 12 13 14 15 16 17 18 19 20 21(patient number)

Patients
Fig. 3. Distribution of the L/DSO of the EOG in 20 affected and fellow intact eyes of 20 patients with ischemic CRVO.
The ratios in Patient 10 were omitted due to unreliable data.

69

M. Inoue et al.

(%)

Affected eye

145

Fellow intact eye

140

Mean ± SD (n = 21)
117.3 ± 10.3
125.9 ± 11.2 **P < 0.05

135

RfFO

130
125
120
115
110
105
100
1

2

3

4

5

6

7

8

9

10

11 12 13 14 15 16 17 18 19 20 21(patient number)

Patients
Fig. 4. Distribution of the RfFO of the EOG in 21 affected and fellow intact eyes of 21 patients with ischemic CRVO.

the 20 patients (95.0%) showed smaller ratios in the
L/DSO in the affected eyes than those in the fellow
healthy eyes. The mean of the L/DFO of all affectedeyes was 1.38 ± 0.37 (SD), and of all fellow intact
eyes was 1.93 ± 0.33. This difference is statisticallysignificant (P < 0.01).

(µV)
300

Affected eye

RfFO
Figure 4 shows the distribution of the RfFO in 21
affected and fellow intact eyes of the 21 patientswith ischemic CRVO. Eighteen out of the 21
patients (85.7%) showed smaller values in the RfFO

Fellow intact eye

250

Mean ± SD (n = 21)85.6 ± 52.7
168.9 ± 60.5 **P < 0.01

dfFO

200

150

100

50

0
1

2

3

4

5

6

7

8

9

10

11 12 13 14 15 16 17 18 19 20 21(patient number)

Patients
Fig. 5. Distribution of the dfF0 of the EOG in 21 affected and fellow intact eyes of 21 patients with ischemic CRVO.

70

EOG slow and fast oscillations in CRVO

Affected eye

Mean ± SD (n = 21)
15.0 ± 8.8*
22.3 ± 8.0*P < 0.01

Fellow intact eye

(%)
40
35

df/mFO

30
25
20
15
10
5
0
1

2

3

4

5

6

7

8

9

10

11 12 13 14 15 16 17 18 19 20 21(patient number)

Patients
Fig. 6. Distribution of the df/mFO of the EOG in 21 affected and fellow intact eyes of 21 patients with ischemic
CRVO.

eyes. The mean of the df/mFO of all affected eyes
was 15.0 ± 8.8%, and of all fellow intact eyes was
22.3 ± 8.0%. This difference was statisticallysignificant (P < 0.01).

in the affected eyes than those in the fellow healthyeyes. The mean of the RfFO of all affected eyes was
117.3 ± 10.3%, and of all fellow intact eyes was
125.9 ± 11.2%. This difference was statisticallysignificant (P < 0.05).

dfFO
Figure 5 shows the distribution of the dfFO in 21
affected and fellow intact eyes of the 21 patientswith ischemic CRVO. Twenty out of the 21 patients (95.2 %) showed smaller values in the dfFO in
the affected eyes than those in the fellow healthyeyes. The mean of the dfFO of all affected eyes was
85.6 ± 52.7 µV, and of all fellow intact eyes was
168.9 ± 60.5 µV. This difference was statisticallysignificant (P < 0.01).

2.5

y = 1.66 + 0.25 log (x)r = 0.46
Correlation analysis (P > 0.05)

L/DSO

2

1.5

df/mFO

1
CF

Figure 6 shows the distribution of the df/mFO in 21
affected and fellow intact eyes of the 21 patientswith ischemic CRVO. Eighteen out of the 21 patients (85.7%) showed smaller values in the df/mFO
in the affected eyes than those in the fellow healthy

0.01

0.1

1.0

Corrected visual acuity at the examination

Fig. 7. Correlation between the L/DSO and corrected visual acuity at the time of EOG examination in 20 affected eyes of 20 patients with ischemic CRVO. CF, counting fingers (estimated to be 0.001).

71

M. Inoue et al.

(%)
150

(µV)
250

y = 125.6 + 7.06 log (x)r = 0.53
Correlation analysis (P < 0.05)

140

200

y = 126.3 + 34.6 log (x)r = 0.51
Correlation analysis (P < 0.05)

dfFO

RfFO

130
120

150

100

110
50

100
90

0
CF

0.01

0.1

1.0

CF

Corrected visual acuity at the examination

On the other hand, a statistically significant
difference was detected in the correlation between
each parameter (RfFO, dfFO and df/mFO) and corrected visual acuity at the time of EOG examination in
the 21 affected eyes of the 21 patients with ischemic
CRVO (P < 0.05) (Figs. 8 to 10).

No significant difference was detected in the correlation between the SO parameter (L/DSO) and corrected visual acuity at the time of EOG examinationin the 20 affected eyes of the 20 patients with ischemic CRVO (P > 0.05) (Fig. 7).

Discussion
Arden and others (1962) postulated that the SO is
related to slower changes in potential that occur as aresult of alterations in the metabolism of the retinal
pigment epithelium. They suggested that normal
magnitudes of corneoretinal potential are dependent on i) normally functioning photoreceptors, ii)
normally functioning retinal pigment epithelium,iii) normal contact between the sensory neuroepithelium and the retinal pigment epithelium and iv)
adequate choroidal blood supply.
Concerning the origin and occurrence of theFO, Steinberg and others (1983) reported the involvement of the retinal pigment epithelium, mainly in its basal membrane. Joseph and Miller (1991)
suggested that the FO might result from delayed hyperpolarization associated with increased electric
resistance in the basal membrane of the retinal pig-(%)

y = 22.55 + 6.39 log (x)r = 0.57
Correlation analysis (P < 0.05)

df/mFO

30

20

10

0
0.01

0.1

1.0

Fig. 9. Correlation between the dfFO and corrected visual acuity at the time of EOG examination in 21 affected eyes of 21 patients with ischemic CRVO. CF, counting fingers (estimated to be 0.001).

Correlations between the SO parameter andcorrected visual acuity and between each FO
parameter and corrected vision

CF

0.1

Corrected visual acuity at the examination

Fig. 8. Correlation between the RfFO and corrected visual acuity at the time of EOG examination in 21 affected eyes of 21 patients with ischemic CRVO. CF, counting fingers (estimated to be 0.001).

40

0.01

1.0

Corrected visual acuity at the examination

Fig. 10. Correlation between the df/mFO and correctedvisual acuity at the time of EOG examination in 21 affected eyes of 21 patients with ischemic CRVO. CF,
counting fingers (estimated to be 0.001).

72

EOG slow and fast oscillations in CRVO

ment epithelium. This delayed basal membrane hyperpolarization may be caused by a decrease in intracellular chloride of the retinal pigment epithelium, which is linked to the light-induced drop in
subretinal potassium concentration (Joseph andMiller, 1991).
In the present study, results showed that the L/
DSO, the RfFO, the dfFO and the df/mFO were significantly decreased in the affected eyes of the patients
as compared with the fellow intact eyes. These results suggest that with regard to SO and FO origin
and occurrence, the outer layer of the retina, especially the basal membrane of the retinal pigment
epithelium or the choroid may be involved in the
etiology of CRVO. These findings correlate withthe grade of microcirculatory disturbance or ischemia in the inner layer of the retina.
As for the influence of retinal bleeding, a decrease in illuminating volume may bring an indirect
or direct influence on the EOG responses, especially in patients with hemorrhagic or ischemic CRVO.
Its influence seems to be very small and negligible
in these patients because their retinal bleeding remains flame-shaped in their fundi.
The EOG responses may be affected by changes
in the retrobulbar circulation due to a systemic hypertensive condition more or less associated withocclusive retinal vascular diseases and/or arterial
blood flow characteristics, that is, reduction ofblood flow velocities in the central retinal and ophthalmic arteries especially in patients with ischemic
CRVO, which may be partly related to secondarychanges in the retrobulbar circulation as a result ofenhanced arterial resistance following CRVO
(Anunduk et al., 1999).
With regard to influences from anemia or
ischemia, elevation of the osmotic pressure in thesubretinal space may bring an unstable retinal pigment epithelium. Decrease of the oxygen quotient
may bring a functional insufficiency in the outer
retinal layers (Honda, 1996). An increase in thevolume of ammonia in the ischemic retina may
bring a functional insufficiency of the whole retina
due to an overflow of glutamic acid. Oxidized
stress after ischemic reperfusion may also bring thesame functional insufficiency of the whole retina
due to an overflow of glutamic acid (Honda, 1996).
Furthermore, the participation of nitric oxide(NO) may disturb the condition of the retinal pigment epithelium and Müller’s cell (Honda, 1996).
An increase in concentration of intracellular calcium ([Ca2+]i) may also bring about cellular damage
in occlusive retinal vascular diseases (Honda,
1996). Other reasons, including morphologicalchanges resembling apoptosis-like cell death, havebeen considered, but the real causes which bringabout such EOG changes in these diseases have notyet been elucidated. In any case, the EOG changes
may be helpful for better understanding of thepathogenesis of CRVO.
It is of note that a statistically significant difference was detected in the correlation between
each FO parameter and corrected visual acuity at
the time of EOG examination of the affected eyes ofthe patients. There was no significance between the
SO parameter and the visual acuity. Rods as well as
cones contribute to the FO (Welber, 1989), whilecones as well as rods contribute to the SO (Arden
and Kelsey, 1962; Gouras and Carr, 1965). Therefore, such a cone-dominated activity on the FO in
this series is currently unexplainable, but it might
be possible to presume that the FO parameters canbe used as indicators for detecting the severity ofmacular functional disturbance and predicting thevisual outcome for this entity.
Generally, visual prognosis is obviously poorer in ischemic CRVO than in non-ischemic CRVO
due to severe retinal bleeding and edema especiallyin the macular area. Ischemic CRVO sometimes
leads to the recovery of visual acuity in parallelwith absorption of retinal bleeding and disappearance of cystoid macular edema after panretinal
photocoagulation. Ischemic CRVO often leads tovisual disturbance due to vitreous bleeding causedby neovascularization from the retina and optic disk
as well as macular edema (Kanski, 1989), and maylead to rubeosis iridis and to potentially painful neovascular glaucoma resulting in visual loss in older
persons (Deng et al., 1994; Papakostropoulos et al.,1992).

73

M. Inoue et al.

stract).
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13 Hayreh SS, Klugman MR, Podhajsky P, Kolder HE.
Electroretinography in central retinal vein occlusion.
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14 Henkes HE. Electroretinography in circulatory disturbances of the retina. I. Electroretinogram in casesof occlusion of the central retinal vein or one of its
branches. Arch Ophthalmol 1953;49:190–201.
15 Honda Y. Cellular and molecular biology of ischemic retina. Nippon Ganka Gakkai Zasshi 1996;100:937–955 (in Japanese with English abstract).
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Kumagami T, Setogawa A, et al. Clinical application of fast oscillation of electro-oculogram. Ganka

Further work is required to investigate these
aspects and the variation of the EOG with time, forthe results above represent readings taken at only
one point in the natural history of the condition.
Acknowledgments: The authors thank Professor
Yoshitsugu Inoue, Division of Ophthalmology and Visual Science, Department of Medicine of Sensory andMotor Organs, School of Medicine, Tottori University
Faculty of Medicine, for his generous help.

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Received May 28, 2003; accepted July 16, 2003
Corresponding author: Akihiko Tamai, MD

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