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Optic nerve head

The posterior segment of the eye contains vitreous humor (a clear jelly-like substance), the retina, the retinal vasculature, and the optic nerve head. The retina transforms light energy... [Pg.912]

Optic nerve head (optic disc) cupping. [Pg.913]

Diffuse thinning, focal narrowing, or notching of the optic nerve head rim. [Pg.913]

Optic nerve head and nerve fiber layer changes occur before visual field changes can be detected. [Pg.913]

Glaucomas are ocular disorders characterized by changes in the optic nerve head (optic disk) and by loss of visual sensitivity and field. [Pg.732]

Differential gene expression in astrocytes from human normal and glaucomatous optic nerve head analyzed by cDNA microarray, GLIA, 38, 45-64, 2002. [Pg.185]

FIGURE 24.1 Ocular and periocular tissues. EL, eyelid DD, drug droplet COR, cornea AC, anterior chamber PC, posterior chamber AOF, aqueous outflow tract (trabeculum meshwork and Schlemm canal) BCNJ, bulbar conjunctiva PCNJ, palpebral conjunctiva FCNJ, fornical conjunctiva FNX, fornix (conjunctival sac/cul-de-sac) SC, sclera IR, iris CB, ciliary body CHOR, choroid RET, retina ONH, optic nerve head V, vitreous L, lens Z, lens zonulae ORF, orbital fat. [Pg.492]

Hofman, P., et al. 2001. Lack of blood-brain barrier properties in microvessels of the prelaminar optic nerve head. Invest Ophthalmol Vis Sci 42 895. [Pg.519]

Fig. 5.1. Retinal section near the optic nerve head showing persistent hyaloid vessels in an ROP mouse. Such regions are excluded from retinal vascular endothelial cell enumeration. Fig. 5.1. Retinal section near the optic nerve head showing persistent hyaloid vessels in an ROP mouse. Such regions are excluded from retinal vascular endothelial cell enumeration.
As demonstrated with fluorophotometry, timolol acts predominantly by decreasing the production of aqueous humor and does not significantly alter facility of outflow. Most studies support the view that both short-term and long-term administration of timolol do not alter optic nerve head circulation or produce retrobulbar hemodynamic changes. The ocular hypotensive effect of timolol is additive to most other therapies, including outflow agents (e.g., pilocarpine) and inflow agents (e.g., dorzolamide, brinzolamide, apraclonidine, and brimonidine). When added to latanoprost, timolol and most other P-blockers further reduce lOP approximately 2 mm Hg. This reduction is less than that attained by topical CAIs such as dorzolamide (Table 10-2). [Pg.147]

Figure 22-12 (A) Compensated edema in a case of pseudotumor cerebri. (B) Noncompensated papilledema in a case of acute aqueductal stenosis. (C) PseudopapUledema secondary to buried drusen of the optic nerve head. Figure 22-12 (A) Compensated edema in a case of pseudotumor cerebri. (B) Noncompensated papilledema in a case of acute aqueductal stenosis. (C) PseudopapUledema secondary to buried drusen of the optic nerve head.
Characteristics of the vision loss can aid in the diagnosis of demyelinating optic neuropathy. The vision loss is progressive, is maximal in 1 week, and achieves variable recovery within 4 to 6 weeks. The reduction in vision frequently is accompanied or preceded by periocular pain on movement of the eye. Color vision often is severely impaired, and visual fields most commonly reveal a relative central scotoma. The ophthalmoscopic picture is usually one of a normal optic nerve head, because most commonly the optic neuropathy is behind the globe and thus is called retrobulbar optic neuritis. When there is optic disc swelling, it is known as papillitis. [Pg.369]

The clinician should suspect toxic optic neuropathy in any case of bilateral painless and symmetric loss of vision with normal or sluggish pupils. Because of the symmetric nature of the accumulation of toxins in the optic nerve head, pupillary fibers of either eye are equally affected and thus no RAPD is produced. [Pg.371]

Clinical features of ARN must include (1) focal well-demarcated areas of retinal necrosis located in the retinal periphery, (2) rapid circumferential progression of necrosis, (3) evidence of occlusive vasculitis, and (4) moderate to severe anterior chamber and vitreal inflammation. Mild presentations may manifest low-grade anterior chamber inflammation with or without blurred vision, whereas severe cases may include episcleritis, scleritis, and pain on eye movement. Early clinical findings include anterior and posterior uveitis, keratic precipitates, and presence of vitreous cells. Within several days to weeks, the patient develops dramatic progressive retinal whitening in multifocal and confluent patches, vasculitis of both retinal arteries and veins, and possible optic nerve head... [Pg.620]

Structural Assessment of the Optic Nerve Head and Retinal Nerve Fiber Layer... [Pg.676]

Assessment of the optic nerve head and retinal nerve fiber layer should occur for all glaucoma patient and glaucoma suspects. [Pg.678]

Indirect ophthalmoscopic assessment of the optic nerve head and retinal nerve fiber layer at the slit lamp should, whenever possible, be augmented by other techniques such as direct ophthalmoscopy, retinal photography, and/or scanning laser ophthalmoscopy. [Pg.678]

Vertical cupping of the optic nerve head Pattern standard deviation on visual fields Thin central corneal thickness < 555 mcm... [Pg.686]


See other pages where Optic nerve head is mentioned: [Pg.912]    [Pg.912]    [Pg.914]    [Pg.921]    [Pg.921]    [Pg.91]    [Pg.182]    [Pg.182]    [Pg.2072]    [Pg.494]    [Pg.498]    [Pg.117]    [Pg.247]    [Pg.477]    [Pg.74]    [Pg.304]    [Pg.309]    [Pg.335]    [Pg.364]    [Pg.368]    [Pg.619]    [Pg.657]    [Pg.671]    [Pg.674]    [Pg.676]    [Pg.676]    [Pg.676]    [Pg.676]    [Pg.677]    [Pg.679]    [Pg.685]   
See also in sourсe #XX -- [ Pg.185 ]




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