Porth's Essentials of Pathophysiology, 4e

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Disorders of Special Sensory Function: Vision, Hearing, and Vestibular Function

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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. 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. Disorders of Neural Pathways and Cortical Centers