Porth's Essentials of Pathophysiology, 4e - page 987

C h a p t e r 3 8
Disorders of Special Sensory Function: Vision, Hearing, and Vestibular Function
969
high-frequency ultrasound may be used in some cases
to destroy the ciliary epithelium and reduce aqueous
humor production.
Angle-Closure Glaucoma
Angle-closure glaucoma results from occlusion of the
iridocorneal angle itself, impairing access to the drainage
aqueous humor (see Fig. 38-11C). An acute attack is
often precipitated by pupillary dilation, which causes
the iris to thicken, thus blocking the circulation between
the posterior and anterior chambers.
6,25,34,35
Angle-
closure glaucoma usually occurs as the result of an
inherited anatomic defect that causes a shallow anterior
chamber. It is more commonly seen in people of Asian
or Inuit (Eskimo) descent and in people with hyperopia.
This defect becomes exaggerated in older adults as the
peripheral iris is anteriorly displaced by the increase in
lens thickness that occurs with aging.
Clinical Manifestations.
Manifestations of acute angle-
closure glaucoma are related to sudden, intermittent
increases in intraocular pressure. These occur after
prolonged periods in the dark, emotional upset, and
other conditions that cause extensive and prolonged
dilation of the pupil. Administration of pharmacologic
agents, such as atropine, that cause pupillary dilation
(mydriasis) also can precipitate an acute episode.
Attacks of increased intraocular pressure are manifested
by ocular pain and blurred or iridescent vision caused
by corneal edema. The pupil may be enlarged and fixed.
Symptoms are often spontaneously relieved by sleep and
conditions that promote pupillary constriction. With
repeated or prolonged attacks, the eye becomes reddened,
and edema of the cornea may develop, giving the cornea
a hazy appearance. A unilateral, often excruciating,
headache is common. Nausea and vomiting may occur,
causing the headache to be confused with migraine.
Subacute angle-closure glaucoma is characterized
by short episodes of elevated intraocular pressure
that subside spontaneously. There are recurrent short
episodes of unilateral pain, conjunctival redness,
and blurring of vision associated with halos around
lights. Attacks often occur in the evenings and resolve
overnight.
34
Examination between attacks may show
only a narrow anterior chamber angle. Although the
episodes resolve spontaneously, there is accumulated
damage to the anterior chamber angle. Subacute angle
closure may also progress to acute angle closure.
Diagnosis and Treatment.
Acute angle-closure
glaucoma is an ophthalmic emergency that must be
differentiated from conjunctivitis, uveitis, or corneal
disorders. Treatment is initially directed at reducing
the intraocular pressure, usually with pharmacologic
agents. Once the intraocular pressure is under control, a
laser peripheral iridotomy may be performed to create a
permanent opening between the anterior and posterior
chambers, allowing the aqueous humor to bypass the
pupillary block. The anatomic abnormalities responsible
for angle-closure glaucoma are usually bilateral, and
prophylactic surgery is often performed on the other eye.
 Congenital and Infantile Glaucoma
Infantile (congenital) glaucoma is defined as glaucoma
that begins within the first 3 years of life.
34,38
It can occur
as a primary or secondary condition. Primary infantile
glaucoma is caused by an isolated anomaly in development
of the anterior chamber. In secondary glaucoma, other
ocular defects or systemic disorders are present.
The clinical manifestations of infantile glaucoma
include excessive lacrimation (tearing), conjunctival
injection (redness of the eye), photophobia (sensitivity
to light), and blepharospasm (eyelid squeezing). Affected
infants tend to be fussy, have poor eating habits, and rub
their eyes frequently. Because the sclera and cornea are
more elastic in early childhood than later in life, chronic
elevation of the intraocular pressure causes enlargement
of the entire optic globe, including the cornea, and
development of what is termed
buphthalmos
(“ox eye”).
Diffuse edema of the cornea usually occurs, giving the
eye a grayish-white appearance. Children with unilateral
glaucoma generally present earlier because differences in
the corneal size between the two eyes canbe noticed.When
both eyes are affected, the parents may not recognize
the increased corneal size. Early surgical treatment is
necessary to prevent blindness. Many children require
several surgeries, as well as long-term medical therapy to
maintain a lowering of their intraocular pressure.
Disorders of Neural Pathways
and Cortical Centers
Full visual function requires the normally developed
brain-related functions of photoreception and the pupil-
lary reflex. These functions depend on the integrity of
all visual pathways, including retinal circuitry and the
pathway from the optic nerve to the visual cortex and
other visual regions of the brain and brain stem.
16,24
Visual information is carried to the brain by axons
of the retinal ganglion cells, which form the optic nerve.
The two optic nerves meet and fuse in the optic chiasm,
beyond which they are continued as the optic tracts
(Fig. 38-13). In the optic chiasm, axons from the nasal
retina of each eye cross to the opposite side and join
with the axons of the temporal retina of the contralat-
eral eye to form the optic tracts.
Fibers of the optic tracts synapse in the lateral
geniculate nucleus (LGN) of the thalamus. Axons from
neurons in the LGN form the optic radiations that
travel to the primary visual cortex in the occipital lobe.
The pattern of information transmission established
in the optic tract is retained in the optic radiations.
For example, the axons from the right visual field,
represented by the nasal retina of the right eye and the
temporal retina of the left eye, are united at the chiasm.
They continue through the left optic tract and left optic
radiation to the left visual cortex (area 17), which is
located in the occipital lobe of the brain (Fig. 38-14).
Immediately surrounding the visual cortex are the visual
association cortices (areas 18 and 19), which function in
adding meaningfulness to the visual experience.
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