NBEO TMOD key terms

Reduced best-corrected acuity in one or both eyes caused by abnormal visual experience during development, with no structural cause explaining the loss. Treated by correcting refractive error, forcing use of the weaker eye, and removing obstacles such as cataract.

Misalignment of the eyes in which the visual axes do not intersect at the same fixation point. Classified by direction as esotropia, exotropia, hypertropia, or hypotropia, and by constancy as intermittent or constant. May cause diplopia or suppression.

A condition in which the two eyes have unequal refractive power, typically differing by at least one diopter of sphere or cylinder. It can disrupt binocular development and is a common cause of unilateral refractive amblyopia in children.

The developmental window in early childhood during which the visual system remains sensitive to abnormal input. Deprivation or misalignment during this time can cause lasting amblyopia, and treatment is most effective before the window closes.

A cortical adaptive mechanism in which the visual input from one eye is actively ignored to avoid diplopia or confusion. In strabismus it is typically scotomatous in the deviated eye and can be detected with tests such as the Worth four-dot.

A binocular alignment test in which one eye is occluded while the other fixates, and the uncovered eye's movement is observed. A refixation movement reveals a manifest deviation; the alternate cover test reveals the total deviation including latent components.

A latent misalignment of the eyes that is held in check by fusion and only becomes apparent when binocular fusion is disrupted, as during alternate cover testing. It is asymptomatic in most people but may decompensate under stress or fatigue.

An inward turn of one or both eyes triggered by the accommodation reflex, most often in hyperopic children whose focusing effort drives convergence. Treatment begins with full hyperopic correction; remaining deviation may respond to bifocals or surgery.

The fluid pressure inside the eye, determined mainly by the balance between aqueous humor production and outflow. Normal ranges roughly 10 to 21 mmHg, but glaucoma can occur at any pressure, so a single reading must be interpreted with corneal thickness and optic nerve findings.

A group of optic neuropathies characterized by progressive retinal ganglion cell loss and characteristic optic disc cupping, often with visual field loss. Intraocular pressure is the major modifiable risk factor, but the disease can occur at statistically normal pressure.

The proportion of the optic disc occupied by the central cup, estimated during funduscopy. Enlargement, asymmetry between eyes, or progressive increase raises suspicion for glaucoma and prompts comparison with baseline imaging and visual fields.

A technique using a mirrored contact lens to view the anterior chamber angle and classify it as open or closed. It is essential for distinguishing open-angle from angle-closure mechanisms and for identifying pigment or neovascular changes before treatment decisions.

Occlusion of the anterior chamber angle by iris tissue, obstructing aqueous outflow. Chronic forms can silently damage the optic nerve, while acute attacks present with severe pain, halos, and a mid-dilated pupil and require urgent pressure-lowering treatment.

The thickness of the cornea measured centrally, which affects how applanation tonometry readings are interpreted. Thinner corneas tend to yield lower readings than true pressure and are themselves associated with greater glaucoma risk.

The total area a person can see while the eye is fixed on a central point, mapped by perimetry. Defects are described by their pattern, such as arcuate, altitudinal, or central, and their pattern helps localize damage along the visual pathway.

A noninvasive imaging method using low-coherence light to produce cross-sectional images of the retina and optic nerve. It quantifies retinal nerve fiber layer and ganglion cell layers, supporting early detection and monitoring of glaucoma and macular disease.

Microvascular damage to the retina from chronic hyperglycemia, ranging from nonproliferative stages with microaneurysms, hemorrhages, and exudates to proliferative disease with neovascularization. Sight-threatening complications include macular edema and vitreous hemorrhage.

Fluid accumulation within the macula causing thickening and blurred or distorted central vision. It is a leading cause of vision loss in diabetic retinopathy and other vascular diseases, detected by slit-lamp biomicroscopy and quantified with optical coherence tomography.

Growth of new, fragile blood vessels in response to retinal ischemia, appearing at the disc, elsewhere on the retina, or on the iris. These vessels bleed easily and can cause tractional detachment or neovascular glaucoma, requiring urgent referral.

The advanced stage of ischemic retinal disease in which neovascularization develops, threatening vision through hemorrhage, fibrosis, and retinal detachment. Management involves panretinal photocoagulation or anti-VEGF therapy and coordinated care with the treating physician.

Degeneration of the macula in older adults, classified as dry, with drusen and geographic atrophy, or wet, with choroidal neovascularization. Wet disease causes rapid central vision loss and requires prompt anti-VEGF treatment.

A grid pattern used for monocular self-monitoring of central vision. New distortion, missing areas, or scotomas may signal choroidal neovascularization or macular edema and warrant urgent dilated examination.

An asymmetric pupillary response in which the affected eye constricts less when light is swung to it, indicating optic nerve or extensive retinal dysfunction. Detected with the swinging flashlight test, it helps distinguish optic neuropathy from media opacity.

Inflammation of the optic nerve, often presenting with subacute unilateral vision loss, pain on eye movement, color desaturation, and an afferent pupillary defect. It may be the first sign of demyelinating disease and warrants neurological evaluation.

Bilateral optic disc swelling caused by raised intracranial pressure, typically preserving normal acuity early while enlarging the blind spot. It requires urgent neuroimaging and evaluation for causes such as mass lesions or venous sinus thrombosis.

Diffuse or localized redness of the conjunctiva or sclera from vasodilation. The differential spans benign conjunctivitis to sight-threatening keratitis, uveitis, and angle closure, so pain, photophobia, and reduced acuity guide urgency.

Inflammation of the cornea, causing pain, photophobia, tearing, and often a visible opacity or epithelial defect. Bacterial, viral, and contact-lens-related forms require slit-lamp evaluation with fluorescein and timely antimicrobial treatment.

Application of fluorescein dye with cobalt blue illumination to highlight corneal epithelial defects, which appear bright green. It is central to diagnosing abrasions, ulcers, and herpes simplex dendrites and to assessing contact lens complications.

Any mismatch between the eye's optical power and its axial length that prevents light from focusing on the retina, including myopia, hyperopia, and astigmatism. It is corrected with spectacles, contact lenses, or refractive surgery.

A refractive state in which unaccommodated light focuses behind the retina, requiring accommodation to see clearly. Children with high hyperopia may develop accommodative esotropia or refractive amblyopia if uncorrected.

A multifactorial disorder of the ocular surface characterized by tear film instability and hyperosmolarity, producing burning, grittiness, and fluctuating vision. Management proceeds from lubricants and lid hygiene to anti-inflammatory and punctal occlusion therapy.

The interval between a complete blink and the first dry spot in the tear film after fluorescein instillation. Shortened values indicate instability and support the diagnosis of evaporative or aqueous-deficient dry eye.

A ranked list of possible conditions consistent with a patient's history and findings, ordered by likelihood and danger. It directs which tests to order and prevents premature closure on a single explanation.

A structured course of action derived from the diagnosis, specifying treatment, follow-up interval, monitoring parameters, and referral triggers. It should reflect patient goals, comorbidities, and the level of care appropriate to the setting.

Predefined findings that mandate escalation to a specialist or emergency setting, such as sudden vision loss, afferent pupillary defect, or suspected angle closure. Clear criteria reduce delay in sight-threatening conditions.

Measures of a test's ability to identify people with and without a condition, respectively. They determine how a result shifts the probability of disease and guide whether a test is useful for screening or confirmation.

The probability that a person with a positive test result actually has the condition. It depends on disease prevalence as well as test accuracy, so the same test performs differently in high-risk and low-risk populations.