HYPERM ETROPIA AND HETEROTROPIA. 
BY 
HOWARD F. HANSELL, M.D., 
OF PHILADFI.V'UA. 
FROM 
THE MEDICAL NEWS, 
October 13, 1894. [Reprinted from The Medical News, October 13, 1894.] 
HYPER METROPIA AND H E T E R 0 T R 0 PI A1 
By HOWARD F. HANSELL, M.D., 
• OF PHILADELPHIA. 
The subject of this communication has been in 
part presented to the profession in two papers, 
"The Treatment of Internal Squint," Annals of 
Ophthalmology, January, 1894, and "A Cause of 
Failure in the Surgical Treatment of Internal 
Squint," read by title before the Pennsylvania State 
Society, May 16, 1894. I desire now to bring it, 
modified and strengthened by added experience, 
before this Society, with the hope that a discussion 
may be elicited by which its value as a statement of 
actual existing conditions and as an explanation of 
those conditions may be determined. I submit the 
following two propositions : 
1. In constant, or monocular squint, due to hyper- 
metropia, when one and the same eye is always 
used in fixation, the second eye is invariably turned 
upward as well as inward. 
2. In concomitant, or alternating squint, due to 
hypermetropia, when either eye is used indifferently 
for fixation, the squinting eye is invariably turned 
upward as well as inward, and, with alternation of 
1 Read before the American Ophthalmological Society at 
Washington, May, 1894. 2 
fixation, the upper deviation is transferred simul- 
taneously with the inward deviation. 
Both propositions may be included in one state- 
ment ; namely, that functional esotropia, or purely 
lateral deviation of the visual axes, is never found 
alone, but is always associated with hypertropia. 
I make these assertions with a certain amount of 
diffidence and hesitation, for, while I have been 
unable to find their equivalents in my reading, it 
seems improbable that these facts have escaped the 
observation of the many careful investigators who, 
following Donders' lead, have so thoroughly studied 
the etiology of functional strabismus, and I fear that 
my own researches into literature have been too 
limited. 
I have found allusions to an upward squint com- 
plicating convergence, and in Stevens' studies, pub- 
lished in the Archives, attention has been called to 
the same condition ; but in no text-book or mono- 
graph with which I am familiar is it positively stated 
that the two must be invariably associated, nor has 
any author, so far as I know, who has mentioned the 
upward squint as complicating the internal, sug- 
gested an explanation. 
If we accept Donders' theory of hypermetropic 
squint, which is, I believe, universally admitted as 
correct, and we pursue his line of reasoning to its 
logical and physiologic conclusion, we shall have 
a satisfactory explanation not only for the existence 
of the hypertropia, but also a sufficiently convincing 
reason for the clinical fact that esotropia cannot be 
caused by hypermetropia unless hypermetropia also 
cotemporaneously develops hypertropia. 3 
Pathologic convergence is induced through exces- 
sive action of the ciliary muscles, by reason of the 
anatomic and physiologic relation of the nuclei of 
the ciliary and interni, when the bounds of relative 
convergence and accommodation have been over- 
stepped. But the nuclei of other branches of the 
third nerve participate with the convergent nuclei 
in this excitation, as is shown in the pupillary con- 
traction. 
Now, the elevators of the cornea are the superior 
rectus and the inferior oblique, and both are supplied 
with motor force from the third nerve. The depres- 
sors of the cornea are the inferior rectus and the 
superior oblique, only one of which receives impulse 
from the third. Therefore, excessive stimulation, 
or hypermetropic stimulation, if I may be allowed 
to use the expression, must induce not only over- 
action of the interni, but also of all the muscles 
supplied by the motor oculi. As the external 
recti cannot maintain lateral equilibrium, the ele- 
vators are for the same reason only in part antago- 
nized by the depressors, and the cornea is rolled 
inward and upward. Hence, when the visual axis 
of one eye crosses that of the other within infin- 
ity, it must be on a higher plane. 
These propositions have been verified by clinical 
observation. In every case, without exception, that 
has come under my care during the past few months, 
in which I have been able to induce the patient to 
become cognizant of the image which falls on the 
retina of the squinting eye, perhaps twenty-five or 
thirty in number, he has described its position as 
homonymous and on a lower level than that of the 
fixing eye. 4 
No insurmountable difficulty has been encountered 
in discovering the false image. It has demanded, 
however, patience and perseverance, and the use of 
glasses of different colors-the true image blurred 
by a dark blue, and the false changed by a bright- 
red glass. It has occasionally been necessary in the 
early efforts to bring the false image nearer to the 
true by prisms, bases out, or to place the light nearer 
to the patient than twenty feet. 
The final and determining tests have always been 
made without artificial deflection of the false image, 
so that no doubt as to its horizontal plane could 
arise from a possible oblique turning of the prism 
thus used. Rarely, cases may be found in which the 
projection is false, when, for instance, in conver- 
gence the images are heteronymous and no deduc- 
tion can be drawn from the patient's answers. Here 
the observer must rely upon objective examination 
of the deviation of the squinting eye, and close in- 
spection will reveal both esotropia and hypertropia. 
Further, I believe the application of the same 
principle can be extended to an elucidation of the 
etiology of hyperphoria as well as hypertropia, and 
help us to a clearer comprehension than we now 
have of the origin of this perplexing condition. 
The bases of argument must again rest upon Bon- 
ders' theory of hypermetropic squint. If hyperme- 
tropia in its higher grades can produce a positive 
deviation of the visual axes, it follows that, in the 
lower grades, it is responsible for tendencies to 
deviation, or "phorias," and, logically, the tend- 
ency cannot be limited to esophoria, but must in- 
clude hyperphoria. 5 
The influence of the ciliary muscle in overcom- 
ing the low grades of hypermetropia and astigma- 
tism in the young is not sufficiently great to destroy 
the extra-ocular balance, and the visual axes are 
maintained in their binocular relation at a cost of 
nerve-energy that, in patients of neurotic disposition, 
is followed or accompanied by severe reflex disturb- 
ances. But it manifestly produces a corresponding 
overaction of the other muscles under the control of 
the third nerve, or a tendency to deviate from 
equilibrium. In persons of middle age, when pres- 
byopia is commencing and the range of relative 
accommodation and convergence is limited by loss 
of accommodation through stiffening of the lens, 
the effort at contraction of the ciliary muscle, or 
the nerve-power, is, however, unchanged from that 
of earlier life, and thus the other branches of the 
third are stimulated in their accustomed degree. 
Since, as has been shown, this action includes other 
than the internal muscles, we have every reason to 
believe that the asthenopia is muscular and not 
accommodative, because better vision or less error 
of refraction in one eye will determine esohyper- 
phoria of the other. 
This hypothesis, more rational than any that has 
been proposed in explanation of the muscular anom- 
alies so frequently associated with hypermetropia, 
receives confirmation in the effect of paralysis of 
accommodation and the optic correction of the 
error of refraction, both in heterotropia and hetero- 
phoria. In the former, the cure of the disjointed 
muscular action by these means alone has been per- 
haps the most persuasive argument to the universal 6 
acceptance of the truth of Bonders' theory ; and in 
the latter, correction of hypermetropia and astig- 
matism has been amply demonstrated to be quite 
sufficient treatment in the great majority of cases 
not only for the accommodative, but for the muscu- 
lar asthenopia, as is so frequently demonstrated by 
the gradual, and in some cases immediate, disappear- 
ance of the symptoms, and by the restoration of 
equilibrium according to the tests commonly em- 
ployed. 
Before advising operation in hyperphoria, we must 
therefore be convinced that it is a permanent and 
real condition, independent of and uninfluenced by 
the use of the accommodation, and cannot be trans- 
ferred from one eye to the other. We may be led 
into error of diagnosis, even in hyperphoria, by the 
fact that the hypermetropic patient under the test 
by artificial horizontal diplopia involuntarily or 
unconsciously fixes at the moment with one eye, 
and having determined in our own mind that a right 
or left hyperphoria is present, all subsequent tests 
seem to confirm the impression. A constant hyper- 
phoria, just as a constant hypertropia, is plainly 
consistent with the theory advanced, and it is only 
in such cases that operation on the superior rectus, 
either alone or in addition to operation on one or 
both internal, is admissible. 
Recognition of the truth of the two propositions 
presented in the first part of this paper, and accept- 
ance of the hypothesis offered in explanation, will 
necessarily modify the methods commonly employed 
in the surgical treatment of latent and manifest 
strabismus due to hypermetropia. 7 
1. In so-called constant monocular squint, bin- 
ocular fixation can be secured and maintained, un- 
less prevented by amblyopia, only by full correction 
of the optic defect, tenotomy of the interni and 
tenotomy of the superior rectus of the squinting 
eye, and possibly of the inferior rectus of the fixing 
eye. 
2. In alternating squint, vertical equilibrium will 
be restored by correction of the refraction and 
tenotomy of the interni, each muscle divided to 
the same extent. Direct surgical treatment of the 
hypertropia is not indicated under any circum- 
stances. 
The endeavor to secure a cosmetic success by 
confining the tenotomies to the squinting eye only, 
such as extensive section of the internus, conjoined 
with advancement of the externus, as recommended 
by most authorities, is greatly to be deplored. 
3. In hyperphoria, operations to secure vertical 
equilibrium may be made only when it is clearly 
proved that relief from asthenopic symptoms cannot 
be secured by less radical measures. And the in- 
fluence of hypermetropia in causing this condition, 
and the possibility of alternation of fixation trans- 
ferring it from one to the other eye, must be borne 
in mind. 
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