Our results confirm previous reports of binocular enhancement of
contrast sensitivity in normal subjects
10 11 14 and extend
the finding to patients with Duane syndrome. We have confirmed that
patients with Duane retraction syndrome have reduced
stereoacuity,
7 but surprisingly found an increase in the
binocular enhancement of their contrast sensitivities compared to that
in normal control subjects. The ratio of 1.33 in normal subjects is
slightly less than the ratio of 1.4 reported by Campbell and
Green,
10 whereas the ratio of 1.52 in the patients is
greater, although both are within the range of values found in the
literature.
11 We found no significant changes in
enhancement with spatial frequency, confirming previous
findings.
10 14
The increase in binocular enhancement came about, not because the
patients with Duane syndrome had better binocular contrast sensitivity
than normal, but because of a reduction in their monocular contrast
sensitivities. The contrast sensitivity of the affected eye of the
patients is significantly poorer than that of the control subjects.
However, the patients also showed greater binocular enhancement than
normal when the binocular sensitivities were compared to the best
monocular sensitivity, and the finding was therefore not simply due to
changes in the affected eyes of the patients.
Although most patients with Duane syndrome use a head turn to maintain
binocular single vision most of the time, there is nevertheless an
intermittent misalignment of their eyes that is present during the
sensitive period of visual development. It has been shown that there is
a loss of binocularly driven cells in the visual cortex in kittens with
a surgically induced constant squint
15 and in monkeys
reared with a prism-induced optical dissociation of their
eyes.
16 By analogy with these animal experiments, it is
likely that patients with Duane syndrome lose some of their binocularly
driven cells during visual development, and, indeed, some lose
binocular function altogether.
7 A reduction in binocular
cells could account for the reduced stereoacuity, because stereopsis
relies on disparity detection by binocularly driven cells. It is
suggested that the greater binocular enhancement of contrast
sensitivity in these patients could also be explained by their having
fewer binocularly driven neurons. Whereas stereoacuity depends on
binocularly driven cells, it is likely that both monocularly and
binocularly driven cells can be used for the contour recognition
involved in our contrast sensitivity task, provided that sensory fusion
is present. The total number of cortical cells available under
binocular conditions (binocular plus monocular for each eye) would
therefore be the same in the patients and normal subjects. However,
under monocular conditions, only binocular cells plus monocular cells
driven by the open eye would be available
(Fig. 3) . This monocularly available population is smaller in patients with
Duane syndrome than in normal subjects, particularly in the affected
eye. Thus, fewer cells are available to detect the stimulus contours at
contrast threshold, with less availability of spatial and probability
summation across the extent of the stimulus. This could reduce
monocular contrast sensitivities. Under binocular conditions the
increased pool of monocular cells related to the other eye can be
recruited, giving increased binocular enhancement and normal binocular
contrast sensitivity.
The same model can also explain the increase of monocular contrast
sensitivity to be indistinguishable from normal binocular values in
patients with an eye enucleated during early visual development, with
the whole cortical neuronal population becoming available to the
remaining eye.
17 18
It is recognized that this explanation is an oversimplification and
ignores such factors as possible interocular suppression and the
increased activation of binocular cells under binocular conditions
compared to monocular, both of which tend to increase binocular
enhancement. It nevertheless provides an explanation for the apparently
paradoxical combination of reduced stereoscopic function and increased
binocular enhancement of contrast sensitivity in these patients. A
similar increase in binocular enhancement of contrast sensitivity has
recently been described in patients with microtropias and anomalous
binocular single vision, and the same explanation may well
apply.
19 If this explanation of changes in monocularly and
binocularly available populations is applicable, then parallel changes
may be present in monocular and binocular electrophysiological testing.
A companion article
20 describes electrophysiological
experiments that test this possibility in a similar group of patients
with Duane syndrome.