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PATIENT
CARE
Six Signs to Tracing Visual
Field Loss Visual fields can uncover
serious pathologies-if you're attuned to looking for them.
Joseph W. Sowka, O.D. Alan G. Kabat,
O.D.,
Contributing Editors
Vision loss is among our
patients' greatest fears. So, when a patient begins to notice that a portion of
his or her vision is diminished or absent, it can result in a great deal of
anxiety.
In fact,
some adults may be more afraid of losing their vision than they are of dying.
That's why we must always regard any new complaint of visual field loss as an
urgent situation.
In many cases, visual field loss indicates an underlying pathology
such as stroke, brain tumor or even multiple sclerosis.
In this ninth and final installment
of our "Review of Symptoms" series, we'll examine the etiologies of visual
field loss and offer some key clinical pearls for managing this challenging
scenario.
Anatomy
To properly diagnose
field defects and recognize their significance, you must first understand the
anatomy of the visual pathway.
Try to think of the visual pathway as a "highway through the
brain" and visual field defects as a "roadmap" to intraorbital and intracranial
disease.
The
pathway begins as retinal fibers from each eye exit the globe via the optic
nerve. The nerves from each eye course through the orbit and merge to form the
optic chiasm. At this point, decussation, or crossing of fibers occurs.
The temporal fibers
from each eye remain on the ipsilateral side, but the nasal fibers decussate to
the contralateral tract. However, there is no crossing of fibers from superior
to inferior.
From
the chiasm, all fibers from each half of the visual field travel through the
brain on the opposite side. The fibers that constitute the visual field right
of fixation travel post-chiasmally through the left brain, and vice versa.
Beyond the chiasm,
the fibers form the optic tract and terminate in synapses at the lateral
geniculate nucleus. New fibers then course posteriorly through the temporal and
parietal lobes, and ultimately converge within the occipital cortex. We call
this portion of the pathway the optic radiations.
The system becomes more organized as
it proceeds toward the visual cortex, lending additional predictive value to
visual field analysis.
When you're armed with a solid comprehension of the visual pathway
anatomy and the "rules of the road," fields can help you identify or confirm
the etiology of practically any given defect. This series of questions will
help you arrive at a proper diagnosis when analyzing a patient's visual field.
- Is the field loss
unilateral or bilateral? A purely unilateral field defect involves
damage to the eye or optic nerve anterior to the chiasm. Remember that the
post-chiasmal pathway involves fibers from both eyes, so any damage there will
manifest as a bilateral defect.
However, a disease process such as glaucoma
or macular degeneration can simultaneously affect the optic nerve or retina in
both eyes. Always rule out ocular pathology and optic nerve disease before
reviewing the fields in these cases.
- Does the field
defect respect the vertical meridian? Field defects that respect the
vertical meridian indicate chiasmal or retrochiasmal lesions. However, in
end-stage diseases such as glaucoma and chiasmal compression from a pituitary
tumor, the field defect will breach the meridians as complete field loss
ensues.
- Does the field show
a pattern? These visual field defects that characterize specific
disorders are easy to recognize:
Central scotoma. This involves the
central 5 to 50 degrees surrounding fixation. Central scotoma usually indicates
damage to the macular photoreceptors or to the papillomacular nerve fibers at
or within the optic nerve. If the scotoma incorporates the blindspot, the optic
nerve is certainly involved.
Conditions that present with this type of
defect include various maculopathies; ischemic, inflammatory or infectious
optic neuropathies; demyelinating optic neuropathy; toxic/nutritional optic
neuropathy; compressive optic neuropathy; and optic atrophy. Demyelinating
neuropathy may induce an assortment of field defects. The presentation varies
among patients and, sometimes, even between eyes.
Cecocentral scotoma. This
defect extends from the physiologic "blindspot" through and into the point of
fixation. Although a central scotoma may also encompass the blindspot, a
cecocentral scotoma is smaller and typically dumbbell shaped. A cecocentral
loss implicates the optic neuropathies detailed above.
Altitudinal scotoma. These
defects involve the field above or below the point of fixation, but do not
cross the horizontal midline-at least not initially.
Altitudinal
defects may involve or spare fixation, depending on the underlying pathology.
Typically, this type of defect extends to the periphery.
You'll encounter this more
often in anterior ischemic optic neuropathy (AION), demyelinating optic
neuropathy and glaucoma than in other diseases. Retinal disease or detachment
also can present with altitudinal field loss, but this should be easy to
recognize when you perform indirect ophthalmoscopy.
Arcuate scotoma. This is
actually a mild form of an altitudinal defect. It does not involve fixation,
but rather the areas just peripheral to it. Arcuate scotoma is the hallmark of
glaucoma, but it also may indicate optic disc edema or demyelinating optic
neuropathy.
Junctional scotoma. This is the only situation in which
unilateral optic nerve disease results in a bilateral field defect.
Junctional scotoma
is an ipsilateral central scotoma with a contralateral superior temporal
quadrantanopsia. It results from damage to the most posterior optic nerve at
the chiasmal junction, known as anterior genu of Von Wilbrand.
Its presence indicates a compressive
lesion, most commonly a pituitary adenoma with a post-fixed chiasm. However,
recent insights in medicine question the existence of this defect, as
anatomically there is controversy over the existence of the anterior genu of
Von Wilbrand.
Hemianopia and quadrantanopsia. You may describe a visual
field defect as a hemianopia if it involves the field either to the left or
right of the point of fixation, but does not cross the vertical midline.
A quadrantanopsia
is simply a more specialized hemianopia that involves both the vertical and
horizontal midlines.
Hemianopic defects tend to localize to the pathway posterior to
the chiasm.
- If bilateral, is
the defect homonymous? Homonymous visual field defects always
localize to the post-chiasmal visual pathway. When the defect is
non-homonymous, the lesion may be located at either the chiasm or optic nerves,
but no further back.
Bitemporal field loss is the calling card of chiasmal disease.
Recall that the nasal fibers cross within the chiasm, so the damage to this
area will manifest as a loss of temporal field in both eyes.
The etiology of chiasmal disease is
usually compressive and may involve either vascular lesions or neoplasms. The
two most common conditions are pituitary adenoma and craniopharyngioma.
Pituitary tumors
usually present with a bitemporal defect that is initially denser above the
horizontal midline; craniopharyngiomas present with a defect that is initially
denser below. Of course, cases of complete bitemporal hemianopia are not
diagnostic in and of themselves. Neuroimaging can confirm the mass.
Binasal defects
rarely indicate chiasmal disease; rather, they almost always are a sign of
bilateral optic nerve disease (such as glaucoma, chronic papilledema or buried
disc drusen). Although damage to the lateral aspect of the chiasm on both sides
would also produce this defect, there are few conditions capable of causing
this type of lesion. Presumably, the only disorder that you can implicate is
bilateral simultaneous internal carotid aneurysms.
- If the defect is
bilateral and homonymous, which side of the field is affected?
Homonymous defects that affect the left side of the field indicate a
post-chiasmal lesion on the right side of the brain. Conversely, right-sided
field defects indicate post-chiasmal damage within the left side of the brain.
The pathway splits
within the optic radiations as the superior fibers travel within the parietal
lobe and the inferior fibers course through the temporal lobe.
Temporal lobe lesions present with a
superior quadrant loss, sometimes called a "pie in the sky" defect. Parietal
lobe lesions may present with a wedge-shaped, inferior quadrant defect ("pie on
the floor") or may cross the horizontal raphe and present as a complete
hemianopic defect. The explanation: While only inferior fibers pass through the
temporal lobe, all pathway fibers ultimately pass through the parietal lobe in
the region of the parieto-occipital junction. So, the extent of a defect in
parietal lobe disease can vary significantly.
Also consider that the superior and
inferior fibers are segregated within the occipital lobe. Lesions to the
occipital cortex above the calcarine fissure yield inferior defects, and
lesions that strike the cortex below the calcarine fissure yield superior
defects. Hence, true quadrantanopsia is more indicative of disease within the
occipital lobe.
Most post-chiasmal lesions arise from cerebrovascular accident or
stroke. However, they also may occur because of compressive tumors, vascular
anomalies, trauma or demyelinating plaques in multiple sclerosis.
- Is the defect
congruous? In other words, does the field defect of one eye greatly
resemble that of the other eye in shape, extent and laterality? Because the
visual pathway becomes more organized as it proceeds toward the cortex, more
posterior lesions generally demonstrate greater congruity.
The more congruous the visual field
defect, the more posterior in the pathway the lesion is likely to be. In fact,
lesions of the posterior occipital cortex are likely to produce bilateral field
defects nearly identical in shape and size, except for the presence of the
blindspot in one eye. However, you cannot localize a complete homonymous
hemianopia within the visual pathway with any certainty, except to say that it
is posterior to the chiasm.
A complete hemianopic defect
indicates extensive damage involving all the fibers in the pathway on one side
of the brain. This type of damage is just as plausible at the level of the
lateral geniculate nucleus as it is at the level of the parietal lobe or the
occipital cortex.
Of course,
volumes can and have been written on the various other subtleties of pathway
damage. But, what we primary care doctors must always remember is that visual
field defects often are an indication of underlying disease involving the optic
nerve or brain. Even simple confrontation fields can be diagnostic for brain
lesions.
Consider
the anatomy of the visual pathway, the rules of the road, signs, symptoms,
history and, of course, the series of questions discussed here. If you find a
defect, the patient must undergo neuroimaging to find and, hopefully, correct
the disorder or prevent it from getting worse. u
Drs. Sowka and
Kabat are on the faculty at Nova Southeastern University College of Optometry,
Fort Lauderdale, Fla.
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