Strabismus - Fundamentals of Clinical Ophthalmology.pdf

STRABISMUS
• Secondly, in the binocular testing of
conjugate movement in the first 3 months of
life, it is not uncommon to see pursuit as a
series of micro-saccades and the pursuit
system not smooth.
• Finally, infants who fail to develop normal
binocular vision will be found to have a latent
fixation nystagmus because of failure to
develop the normal nasotemporal pursuit.
The eyes tend to drift nasally and show fast
phase corrective jerks and the nystagmus
increases if one eye is covered, which is why
this clinical finding is described as latent
nystagmus. The observation requires a visually
attentive child and careful observation by the
clinician. Any disturbance of clear imaging of
visual targets sufficient to interrupt the
development of normal binocular vision in the
first 6 months of life will be accompanied by a
similar nystagmus. It is not confined to
congenital infantile esotropia.
In congenital infantile esotropia (see Chapter 4)
during the first 6 months, there is failure to
establish normal M-neuron connections required
for normal nasotemporal pursuit and pursuit
asymmetry persists. 15 For this reason when
pursuit asymmetry is present in an adult, it
indicates that strabismus since infancy is likely
and suggests the possibility that the presence of
subnormal vision may be strabismic amblyopia.
The association of amblyopia with disruption of
normal binocular vision is more likely to occur
under the age of 5 or 6 years. Adult patients may
develop strabismus from loss of fusion due to
persistent visual deprivation but they do not
develop amblyopia.
Clinically, it is important to understand eye
movements in the first months of life particularly
if one examines the eyes monocularly. The
infant responds to the information contained
in the M (magnocellular) pathway, showing
preference to targets that move in a temporal to
nasal direction in the visual field. By contrast,
the infant tracks targets poorly that move
temporally with regard to the eye being tested. 13
The difference relates to movement response to
visual stimulus, not the motor pathway. 15 After
3–5 months this nasal bias of visual pursuit is
replaced by symmetrical nasotemporal pursuit
if normal binocular vision develops. The
development of high visual acuity after birth
depends on maturation of synaptic connections,
the visual path and primary visual cortex. The
development of normal binocular vision requires
an equal visual input to the visual cortex from
each eye and during development there is a
competition between the eyes for representation
within the visual cortex. With a balanced input
there would be an associated matching neuronal
connectivity of the information processed from
each eye and the possibility of normal binocular
vision. Therefore a deficit of the visual image
from one of the eyes results in altered neuronal
connectivity and the possibility of breakdown
of binocular vision. Specific clinical examples
include variants of Ciancia syndrome and
strabismus associated with congenital cataract.
Specific clinical examples
Variants of Ciancia syndrome
With malformation of one eye, such as
severe microphthalmos or surgically induced
prenatal absence of one eye in an animal model,
permanent changes can be demonstrated in the
cellular organisation and synaptic connectivity
in the areas of the brain subserving binocular
vision. 16 The lateral geniculate nucleus has an
absence of representation of the eye removed
and additional connections are formed between
the intact eye and the geniculate neurons that
have lost their input. In the visual cortex ocular
dominance columns fail to develop. The
frequent result is an abducting nystagmus in the
sound eye with a null point in convergence
reminiscent of that seen in Ciancia syndrome
with face turn away from the microphthalmic or
defective eye.
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