How, then, could the 
strabismus have produced such 
a radical change in cortical 
function? To answer this we 
need to consider how the two 
eyes normally act together. 
What the strabismus had 
changed was the relationship 
between the stimuli to the two 
eyes. When we look at a scene, 
the images in the two retinas 
from any point in the scene 
normally fall on locations that 
are the same distance and in 
the same direction from the two 
foveas--they fall on 
corresponding points. If a 
binocular cell in the cortex 
happens to be activated when 
an image falls on the left 
retina--if the cell's receptive 
field is crossed by a dark-light 
contour whose orientation is 
exactly right for the cell--then 
that cell will also be excited by 
the image on the right retina, 
for three reasons: (1) the images 
fall on the same parts of the two 
retinas, (2) a binocular cell 
(unless it is specialized for 
depth) has its receptive fields 
in exactly the same parts of the 
two retinas, and (3) the 
orientation preferences of 
binocular cells are always the 
same in the two eyes. If the eyes 
are not parallel, reason 1 
obviously no longer applies: 
with the images no longer in 
concordance, if at a given 
moment a cell happens to be 
told to fire by one eye, whether 
the other eye will also be 
telling the cell to fire is a 
matter of chance. This, as far as 
a single cell is concerned, 
would seem to be the only thing 
that changes in strabismus. 
Somehow, in a young kitten, 
the perpetuation over weeks or 
months of this state of affairs, 
in which the signals from the 
two eyes are no longer 
concordant, causes the weaker 
of the two sets of connections 
to the cell to weaken even 
further and often for practical 
purposes to disappear. Thus we 
have an example of ill effects 
coming not as a result of 
removing or withholding a 
stimulus, but merely as a result 
of disrupting the normal time 
relationships between two sets 
of stimuli--a subtle insult 
indeed, considering the gravity 
of the consequences.

    In these experiments, 
monkeys gave the same results 
as kittens; it therefore seems 
likely that strabismus leads to 
the same consequences in 
humans. Clinically, in someone 
with a long-standing 
alternating strabismus, even if 
the strabismus is repaired, the 
person does not usually regain 
the ability to see depth. The 
surgeon can bring the two eyes 
into alignment only to the 
nearest few degrees. Perhaps 
the failure to recover is due to 
the loss of the person's ability 
to make up the residual deficit, 
to fuse the two images perfectly 
by bringing the eyes into 
alignment to the nearest few 
minutes of arc. Surgically 
repairing the strabismus aligns 
the eyes well enough so that in 
a normal person the neural 
mechanisms would be 
sufficient to take care of the 
remaining few degrees of fine 
adjustment, but in a strabismic 
person these are the very 
mechanisms, including 
binocular cells in the cortex, 
that have been disrupted. To get 
recovery would presumably 
require protracted 
reestablishment of perfect 
alignment in the two eyes, 
something that requires normal 
muscle alignment plus an 
alignment depending on 
binocular vision.