ACTA O P H T H A L M O L O G I C A 64 (1986)623-631

Characteristics of corneal endothelial cells

in Fu c hs’ heterochromic cycl itis

Hannu I. Alankol, llkka Vuorrel

and K. Matti Saari2

Department of Ophthalmology1 (Head: H. Forsius),

University of Oulu, Oulu
and Department of Ophthalmology2 (Head: K. M.Saari),
University of Tampere, Tampere, Finland

Abstract. We studied the corneal endothelial cells in
14 patients (6 men and 8 women, ranging in age from
15 to 70 years) with unilateral Fuchs’ heterochromic
cyclitis (FHC) by means of specular microscopy. The
healthy fellow eyes of the patients served as control
material. Two affected eyes had undergone an intra-
capsular cataract extraction before specular micro-
scopy. In one patient, the cyclitic eye also had glaucoma.
Changes of the endothelium characterized by intra- and
intercellular dark bodies, larger dark defects spanning
several endothelial cells and bright irregular patchy
areas crossing cell borders on the specular reflex were
found in all eyes with FHC.
Individual cell analysis did not reveal any significant
differences in the endothelial cell density, cell area,
coefficient of variation for cell area, cell perimeter, cell
shape and in the number of endothelial cell apices
between unoperated cyclitic and healthy fellow eyes.
T h e mean cell density was 4.9% lower in the unope-
rated eyes with FHC than in the control eyes. A signifi-
cant negative correlation was observed between the
patients’ age and the cell density both in the healthy and
the cyclitic eyes. On the other hand, the correlation
between follow-up period and cell density was not
statistically significant in the cyclitic eyes. Although
FHC does not seem to accelerate significantly the age-
related cell density reduction, the magnitude of the cell
loss found in the two operated eyes (45.5% and 49.8%)
and in the eye with glaucoma (45.2%) may indicate
altered tolerance against endothelial traumas in this
disease.
Key words: corneal endothelium - Fuchs’ hetero-
chromic cyclitis - morphometry - specular microscopy
- uveitis.
With specular microscopy it is possible to investi-
gate non-invasively the cells of the corneal endo-
thelium in vivo (Laing et al. 1975; Bourne &
Kaufman 1976). Specular microscopy has been
used to study the corneal endothelial cells in acute
and chronic iridocyclitis (Setala 1979a; Olsen
1980a, 1981). Olsen (1981) found typical changes
in the specular appearance of the endothelium in
anterior uveitis. These changes disappeared com-
pletely with other signs of inflammation. In spite
of the qualitative changes seen, quantitative ana-
lysis did not reveal any significant endothelial cell
loss in eyes with acute anterior uveitis (Setala
1979a; Olsen 1980a, 1981). On the other hand,
chronic severe iridocyclitis with mutton-fat keratic
precipitates (Setala 1979a) or recurrent attacks of
anterior uveitis with elevated intraocular pressure
(Olsen 1980a) lowered the corneal endothelial cell
density.
Fuchs’ heterochromic cyclitis is a clinical entity
characterized by a chronic, quiet cyclitis with
minimal flare and cells in the anterior chamber,
small, white keratic precipitates and delicate inter-
posed feathery filaments, diffuse stromal atrophy
and patchy loss of the iris pigment layer, a change
of colour of the iris, absence of posterior syne-
chiae, vitreous opacities, development of compli-
cated cataract and occasionally a secondary glau-
coma (Fuchs 1906; Kimura et al. 1955; Loewen-
feld & Thompson 1973). Abnormal iris vessels
with a small filiform haemorrhage occurring after
paracentesis (Amsler & Verrey 1946) and ischae-

623
mia and leakage of the dye in iris fluorescein
angiograms (Saari et al. 1978a; Berger et al. 1980)
have also been observed.
Since there are reports on endothelial cell
changes in some forms of uveitis and occurrence
of long-standing keratic precipitates and slow
tissue destruction but no detailed information of
the corneal endothelium in FHC, we decided to
study whether there are also changes in endothe-
lial cell moiphology in this disease.
Material and Methods
Our study material consisted of 14 patients with
Fuchs’ syndrome (Table 1). There were 6 males
and 8 females, ranging in age from 15 to 70 (mean
36.5) years. The follow-up period after the first
ocular examination varied between 2 and 14
(mean 6.7) years. Eleven patients had hetero-
chromia. The cyclitis was unilateral in all cases;
the right eye was affected in 7 cases. All affected
eyes showed signs of a quiet, chronic anterior
uveitis with small, grey-white keratic precipitates,
and rarefaction of the iris stroma with changes in
the relief of its anterior surface. The atrophic
changes of the iris were confirmed by infra-red
transillumination stereophotography (Saari et al.
197813) in all cases. Simultaneous bilateral fluores-
cein angiography of the iris (Saari et al. 1978a)
showed fluorescein leakage of the iris vessels in all
of the cyclitic eyes. Each patient had a complicated
cataract, in one patient (Case 12) so dense that the
ocular fundus could not be seen. One patient
(Case 3 ) had had elevated intraocular pressure in
the cyclitic eye treated by pilocarpine and epine-
phrine for 5 years before specular microscopic
examination. Two patients (Cases 13 and 14) had
undergone intracapsular cataract extraction of
the heterochromic eye 4 years (Case 13) and 5
years (Case 14) before specular microscopic exa-
mination. In Case 13 the operation was compli-
cated with a small rupture of the lens capsule, and
in Case 14 small filiform haemorrhage occurred
when the anterior chamber was opened. Vitreous
opacities were seen in eight patients (Table 1). All
eyes had clear corneas.
We photographed the central corneal endothe-
hum of both eyes in all patients using a modified
Bio-Optics LSM-76-2A small-field contact specu-
lar microscope and Kodak Tri-X film. To reduce
image blurring caused by rapid eye movements

Table I.
Summary of clinical data in 14 cases of Fuchs’ heterochromic cyclitis.

Follow-up Keratic Aqueous* Atrophy Com-

Case Cyclitic Hetero- Vitreous
Sex Age period preci- of plicated opacities*
No. years eye chromia*
years pitates* Flare Cells Iris* cataract”

1 M 45 2 L.E. + + - - + + +
2 M 15 4 L.E. + + + + + + +
3 F 48 10 L.E. + + + + + + -
4 F 38 14 L.E. + + f - + + +
5 F 32 6 R.E. + + + - + + +
6 F 17 2 R.E. + + + + + + +
7 F 23 5 RE. + + + + + f +
8 F 31 5 L.E. - + + - + + -
9 M 17 10 L.E. + + + + + + -
10 F 70 13 RE. + + + - + + +
11 F 39 6 R.E. - + + + + + +
12 M 45 4 RE. - + - - + + ..a
1 3b M 49 9 R.E. + + + + + + -
14b M 44 4 L.E. + + - + + + -

* +, Designated symptom was present; -, symptom was absent.

a T h e vitreous could not be seen due to dense cataract.
b I n Cases 13 and 14 the cyclitic eye had undergone intracapsular cataract extraction before specular microscopy.

624
the original flash unit of the microscope was
replaced by one with shorter flash duration. From
3 to 22 (mean 10) photomicrographs were taken
from the central corneal endothelial mosaic in
each eye. The photographic negatives were en-
larged to 8 x 24 cm paper prints. The magnifica-
tion was controlled by copying a micrometer scale
photographed with the specular microscope on
the prints during the enlarging process. Average
cornea-to-print magnification used was 577 times.
We made the qualitative evaluation of the spe-
cular photomicrographs according to the guide-
lines presented by Laing et al. (1979). The quanti-
tative cell features were determined in all cases
using a microcomputer-based individual endothe-
lial cell analysis described earlier in detail by
Alanko (1983). For each eye 60- 100 (mean 94.3)
endothelial cells were analyzed combining data
from 2-7 (mean 4) specular photomicrographs.
The following characteristics of the endothelial
cells were determined: mean cell area, coefficient
of variation for cell area, endothelial cell density
calculated from mean cell area, mean cell peri-
meter, mean number of apices per cell and a
parameter quantitizing the cell shape. This di-
mensionless, size and orientation independent
parameter, called ‘shape deviation’, indicates the
deviation of cell shape from that of the equilateral
hexagon expressed in per cents. If the cell is an
equilateral hexagon in shape the value of the
parameter is zero. If the cell is rounder or more
elongated than the reference shape, this para-
meter gets correspondingly higher positive or
negative values (Alanko 1983). In normal eyes
most of the cells are slightly elongated and the
distribution of the cell shapes is skewed to the left
towards elongated cell shapes (Alanko et al., un-
published data). In all cases the contralateral
healthy eye was used for control. The possible
effect of FHC on the corneal endothelium was
evaluated only in those cases which had not
undergone any intraocular operation (Cases
1-12).
To test the differences between the means of
the analyzed parameters we used the paired t-test.
For the linear correlations Pearsons’ correlation
coefficients were calculated. We considered a
value of P < 0.05 to be statistically significant.

Fag. 1 .
Case 7 : Central corneal endothelium of the healthy left eye (top) and of the right eye with Fuchs’ syndrome
(bottom). Small, dark intracellular spots are more clearly visible in the healthy eye The cyclitic eye shows many
inter- and intracellular dark bodies, smaller than one cell diameter and probably presenting invading inflammatory
cells. I n some areas the cell images are blurred. Cell density: top, 2547 cells/mm2;bottom, 2540 cells/mm2.One scale
division = 10 pm.

40 Acta Ophthal. 64.6 625

 Fig. 2.
Case 3: Central corneal endothelium of the healthy right eye (top) and of the left eye with Fuchs’ syndrome and
secondary glaucoma (bottom). The cyclitic eye shows a large dark defect over 100 pm in diameter and with brighter
central portion, presumably caused by keratic precipitate, and irregular bright patches (arrows). Note elongated cell
shapes in the cyclitic eye. Cell density: top, 2810 cells/mm*; bottom, 1541 cells/mm2. Shape divations: top, - 1.6%;
bottom, -4.7%. One scale division = 10 pm.

Results across the endothelium and often located at the

Qualitative evaluation of the corneal endothelial
photomicrographs of the unoperated eyes (Cases
1 - 12) showed altered appearance of the endo-
thelium in all eyes with heterochromic cyclitis as
compared with the healthy fellow eyes. In cyclitic
eyes areas were seen where the cell boundaries
were not so well defined as in the healthy eyes
(Fig. 1). The endothelial cells in the healthy eyes
were approximately of the same size and shape. In
the cyclitic eyes distinct pleomorphism was ob-
served only in Case 3 (Fig. 2) and in the operated
eyes (Fig. 3). Occasionally, small, dark central
bodies were seen in eyes with FHC but not as
clearly as in the fellow eyes (Fig. 1). Laing et al.
(1979) proposed that these sharp, well-defined
dark bodies present the bases of the endothelial
cilias.
Typically, three groups of specular defects
could be distinguished in cyclitic eyes: 1) dark
bodies, approximately 5 to 15 km in diameter and
round to oval in shape were randomly positioned
cell boundary intersections (Figs. 1 and 3). 2)
large, dark defects with ill-defined boundaries
and occasional bright central reflex, and spanning
several endothelial cells were seen in some frames
(Fig. 2). 3 ) bright, irregular, randomly positioned
patchy structures acrossing the cell borders (Fig.
2).
Qualitative evaluation of the corneal endothel-
ial photomicrographs of the two eyes which had
undergone intracapsular cataract extraction (Ca-
ses 13 and 14) showed similar inter- and intra-
cellular projected dark bodies and bright irregu-
lar patchy structures which were also seen in the
unoperated eyes. However, the endothelium was
pleomorphic, and the cell size was markedly en-
larged as compared with the contralateral healthy
eye (Fig. 3).
Means of analyzed cell parameters of the un-
operated cases (Cases 1-12) are presented in
Table 2. We found no statistically significant dif-
ferences in cell densities ( P = 0.332) and cell areas
( P = 0.599) between the affected eyes and the

626
healthy fellow eyes. The frequency distributions
of cell areas in the cyclitic eyes and the normal
ones skewed similarly to the right (Fig. 4). Neither
did we find any statistically significant difference
when we compared the shape parameter, shape
deviation, in the cyclitic and healthy eyes ( P =
0.052). In both groups the distribution of cell
shapes skewed to the left towards elongated cell
shapes (Fig. 5).
Individual cell analysis showed 45.5% (Case 13)
and 49.8% (Case 14) cell loss in the eyes which had
undergone intracapsular cataract extraction as
compared with the contralateral healthy eyes. In
the unoperated eyes (Cases 1-12) the mean cell
density was 4.9% lower in the cyclitic eyes than in
the healthy ones. There was a negative correlation
between the patient’s age and the cell density both
in the healthy eyes (r = -0.58, P < 0.05) and in
the cyclitic ones (r = -0.76, P < 0.01), whereas
the difference between these correlation coeffi-
cients was not statistically significant ( P > 0.4).
The correlation between the follow-up period and
the central corneal endothelial cell density in the
cyclitic eyes was not statistically significant (r =
-0.29, P > 0.1).
Discussion
The results of this study showed that the typical
specular microscopic findings in FHC include
intra- and intercellularly located blackout areas,
larger dark defects spanning several endothelial
cells and bright, irregular patchy areas super-
imposed on the cell images. However, these find-
ings are not pathognomonic to FHC. Some of
these specular microscopic changes have been
observed earlier in anterior uveitis. The most
frequent changes, intra- or intercellular dark
bodies, resemble those described by Olsen (1981)
in acute anterior uveitis. Also other authors have
reported analogous specular defects in eyes with
uveitis (Laing et al. 1979; Hartmann 1981; Bigar
1982; Hirst et al. 1982; Hirst & Stark 1983). Laing
et al. (1979) presumed that they represent invad-
ing inflammatory cells. Hirst et al. (1982) stated
that these blackout areas correspond most closely
to the scanning electron microscopic observation
of white blood cells on the endothelial surface.
The larger dark defects seen in this study, cover-
ing several endothelial cells and occasionally
showing brighter central portion were similar in

Fig. 3 .
Case 14: Central corneal endothelium of the healthy right eye (top) and of the cyclitic left eye after intracapsular
cataract extraction (bottom). The operated cyclitic eye shows inter- and intracellular dark bodies. The cell size is
markedly enlarged. Cell density: top, 2823 cells/mm2;bottom, 14 17 cells/mm*. One scale division = 10 pm.

40* 627
 Cell features
There was no statistically significant (P > 0.05) difference in cell features
between the affected eyes and the fellow eyes.
appearance to those identified as precipitates by
Olsen (1981) and Hartmann (1981). The cause of
the third type of the endothelial changes, the
bright patches, is not quite clear. Those bright,
irregular areas crossing cell borders may present
leucocytes attached loosely on endothelium (Bigar
1982), endothelial pigment deposits (Laing et al.
1979; Bigar 1982), or they may be reflexes from
the fine cotton-wisp filaments crossing between
the keratic precipitates.
Although the observations in qualitative ana-
lysis were typical and altered specular appearance
was seen in all cases, the individual cell analysis
did not reveal any significant differences in the
analyzed endothelial cell parameters between the
cyclitic and healthy eyes. Our results are in good
agreement with the earlier brief notes on an
unaltered endothelial cell density in eyes with
FHC. Neubauer (1980) reported a cell density of
2800 cells/mm2 in one case with FHC. Kimura
628
Affected eyes Fellow eyes
(1978) cites a study by Hirabayashi in which no
endothelial cell density changes were found in
eyes with Fuchs’ syndrome. In our study the
degrease of the mean cell density in the cyclitic
eyes was 4.9%,a value similar in magnitude to
that of 0.7% found by Setala (1979) in 35 patients
with unilateral uveitis.
Matsuda et al. (1985) observed elongation of
endothelial cells surrounding fresh endothelial
defects. In this study evaluation of the cell shapes
did not reveal any significantly elongated cells in
cyclitic eyes, which would indicate reparation of
endothelial defect in process.
Complicated cataract is frequently found in
eyes with FHC (Kimura et al. 1955; Kimura 1978;
Liesegang 1982). Kimura (1978) suggested that
after cataract surgery corneal oedema occurs
more easily in patients with FHC than in normal
subjects. In another study 29.4% of patients who
had underwent a cataract operation developed
 501
40

<=100150 250 350 450 550 650 750 850 =>950

Cell area, square micrometers
Fig. 4 .
Frequency distribution of cell areas in healthy eyes (solid line) and in unoperated eyes with Fuchs’ syndrome (dotted
line). I n both groups the cell area distributions are skewed similarly to the right toward large cell areas.

c o r n e a l o e d e m a (Liesegang 1982). In this study opacities in t h e posterior cortex or subcapsular

two patients had u n d e r g o n e intracapsular cataract r e g i o n of t h e lens i n t h e cyclitic eye. In t h e
extraction 4 and 5 years before specular micro- o p e r a t e d eyes t h e cell loss was 45.5 and 49.8%
scopic examination, and all o t h e r patients h a d with an endothelial cell density o f 1417 and 1718

VI
-aJ
c

U
4-
0
aJ
0
0
-I-
C
W
U
L
aJ
(L

r - ~1 ~ - I 1 I I
< =-20 -15 -10 -5 0 =>+5
Shape deviation, percents
Fig. 5 .
Frequency distribution of cell shapes in healthy eyes (solid line) and in unoperated eyes with Fuchs’ syndrome
(dotted line). I n both groups the distributions are negatively skewed toward enlongated cells shapes.

629
cells/mm2, respectively. The endothelial cell loss
found in our two cases is higher than the cell loss
of 4-25 % reported after intracapsular cataract
extraction (Drews & Waltman 1978; Olsen 1980b)
and is closer to the values seen after intraocular
lens implantation (Bourne et al. 1981),but still far
from the decompensation limit which may lie
somewhere around 300 cells/mm2 (Waring et al.
1982).
In the present study the greatest endothelial
cell loss in the unoperated cyclitic eye, 45.2%, was
seen in a patient with elevated intraocular press-
ure treated with pilocarpine and epinephrine for
five years before specular microscopy. Also the
cell shapes were elongated in the cyclitic eye,
which may indicate recent endothelial damage. In
this case the endothelial cell density may have
been reduced by elevated intraocular pressure, as
earlier observed in acute glaucoma (Setala 1979b;
Bigar & Witmer 1982) and/or by the long-term
topical epinephrine therapy (Waltman et al.
1977). However, the highest intraocular pressure
of 36 mmHg measured in this case was lower than
the mean intraocular pressure at admission in the
above mentioned studies. Although few, the pres-
ent cases with marked cell loss may indicate that
the endothelium is more vulnerable to equivalent
corneal damages in eyes with FHC than in normal
ones.
I n spite of the altered specular appearance
of the endothelium, Fuchs’ syndrome seems not
significantly accelerate the endothelial cell loss
caused by normal aging. However, our results
may suggest decreased resistance to endothelial
traumas, a finding that prompts carefulness when
intraocular is done in this disease.
Keratic precipitates may disappear after catar-
act extraction or may persist even 35 years post-
operatively (Norn 1968; Loewenfeld & Thomp-
son 1973). In this study the two aphakic patients
still showed specular microscopic changes similar
to those seen in other cyclitic eyes.
Our study indicates that FHC causes corneal
endothelial changes similar to those seen in some
other forms of anterior uveitis. In this study
ocasional inflammatory cells were seen to infil-
trate the corneal endothelium. Our findings sup-
port the recent hypothesis that in FHC there is a
true inflammatory component of immunologic
origin, although a degeneration or an abiotrophy
might be the initial triggering event (O’Connor
1985).
630
Acknowledgments
This study was supported in part by grants from the
Silvia - ja kudospankkisaatio Foundation, the Medical
Research Foundation of Oulu and the Finnish Eye
Foundation (Dr Alanko); and the Medical Research
Council of the Academy of Finland (Dr Saari).
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Received on June 16th, 1986.
Author’s address:
Hannu I. Alanko, M.D.,
Department of Ophthalmology,
University of Oulu,
SF-90220 Oulu 22, Finland.
63 1