Visual change functional correlates

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Normal Vision Changes with Aging: Diagnosis and Management




Decrease in visual acuity

Performing all visual tasks

Increase illumination

Increase contrast


Difficulty with near point tasks

Corrective eyeglasses

Increase illumination

Decrease in contrast sensitivity

Difficulty seeing under conditions of poor lighter (e.g., night driving, church) and poor contrast (e.g., reading a newspaper)




Decrease in dark adaptation

Problems with tunnels, movie theaters, night driving

Sunglasses when outdoors

Take a moment to dark/light adapt before trying to walk

Delayed recovery from glare

Problems with headlights, decreased visual functioning on sunny days

Sunglasses (but not for night driving)

Antireflective lens coating

Hats, visors

Less fluorescent lighting

(Source: Carter, T.L. (September 1994). “Age-related vision changes: A primary care guide. Geriatrics, 49(9), 37-45.)
Classifications of Visual Impairment



Legal blindness

Best visual acuity ≤ 20/200 in the better eye or

Visual filed ≤ 20o

Partially sighted

Best visual acuity ≤ 20/70 in the better eye or

Visual filed ≤ 30o

Functionally visually impaired

When activities of daily living are affected

Best visual acuity ≤ 20/50

(Source: Carter, T.L. (September 1994). “Age-related vision changes: A primary care guide. Geriatrics, 49(9), 37-45.
The four most prevalent age-related ocular diseases and the four leading causes of low vision in the US are:

  • Macular degeneration

  • Open-angle glaucoma

  • Cataract

  • Diabetic retinopathy

Age-Related Macular Degeneration (AMD)

  • Leading cause of irreversible blindness in people 50 years of age or older in the developed world

  • Prevalence: 30% at age 75+; currently 8 million Americans have AMD

  • Risk factors: advanced age, white race, heredity, systemic hypertension, and a history of smoking

  • Only 10% of individuals with macular degeneration have significant functional visual loss.

  • Since the macula is the area for central vision and provides the highest degree of visual resolution, deterioration of this portion of the retina leads to the loss of central vision.

  • Leads to deficits in form recognition and light sensitivity

  • Types of macular degeneration:

    • Dry (non-exudative) macular degeneration

      • Most common (80-90% of cases)

      • Manifested by a progressive loss of retinal and pigment epithelium and gradually increasing central blind spot

      • Untreatable

    • Wet (exudative, or neovascular) macular degeneration

      • Due to accumulation of subretinal blood or exudates (from neovascularization)

      • Can have an acute onset with decreased central vision, metamorphopsia (blurred vision), or a dark spot in the central vision (central scotoma)

      • If found early and not yet in fovea, laser phocoagulation therapy is possible

  • Management (Source: Jager, RD, Mieler, WF, & Miller, JW. (June 12, 2008). NEJM, 358(24), 2606-2617)

    • Antioxidant supplementation (Preser-Vision, Bausch & Lomb): Vitamins C & E, beta carotene, zinc oxide, and cupric oxide.

      • NOTE: Not recommended for those with any smoking history due to increased risk of lung cancer with beta-carotene supplements in current or former smokers. (Source: Gohel, PS, Mandava, N, Olson, JL, & Durairaj, VK.(April 2008). The American Journal of Medicine, 121(4), 279-281.)

    • Lifestyle and dietary modifications

      • Quit smoking

      • Decrease dietary intake of fat

      • Maintain healthy weight and BP

      • Increase dietary intake of antioxidants through foods such as green leafy vegetables, whole grains, fish, and nuts

    • Intravitreal antiangiogenic therapy (injection of antiangiogenic agents directly into the vitreous)

  • Visual rehabilitation for macular degeneration

    • Self-monitor central vision (Amsler’s chart/Amsler’s grid)

    • Magnify the area of central vision

      • Hand-held ocular lenses

      • Video enlargement

      • Microfilm reading systems

      • Increase field illumination



  • Formerly: increased IOP that leads to blindness

  • Now: A group of conditions characterized by eye changes usually associated with increased IOP

  • A progressive optic neuropathy involving characteristic structural damage to the optic nerve and characteristic visual field defects

Changes in IOP:

  • Normal IOP: 10-20 mm Hg and IOP difference of less than 3 mm Hg between eyes

  • Pressures of 20-30 mm Hg will cause gradual damage over the years due to atrophy of the retinal ganglion cell layer.

    • Damage seen on fundoscopy:

      • optic disk shows cupping of the optic nerve head and a decrease in the diameter of the optic vessels

      • as the orange-red area of nerve fiber axons shrinks, the lighter cup in the center grows and the visual field of the patient becomes smaller

    • Changes in the disk are reflected in the patient’s decreased visual acuity

  • Pressures of 40-50 mm Hg can cause much more rapid vision loss due to ischemia of the optic nerve and retinal structures and may even result in vascular occlusion.

  • For example of how vision can change with glaucoma:

  • 5 million people worldwide are blind from glaucoma (World Health Organization)

    • People diagnosed with glaucoma in Third World countries are more likely to progress t blindness due to lack of treatment options

  • In US: 2 million diagnosed with glaucoma

  • High predominance in:

    • African Americans and Asians than Caucasians

    • Females more than males

    • Between ages 55 and 70

Conventional pathway for normal flow of aqueous humor: fluid passes from the posterior chamber through the papillary aperture to the anterior chamber, then to the trabecular meshwork, exiting through Schlemm’s canal and finally into the episleral veins, which drain into the venous system via the facial vein.

Both diagrams taken from: website of National Glaucoma Research, a program of the American Health Assistance Foundation at

Glaucoma Terminology

(Erwin, EA & Mendelson, M. (July 2005) Acute presentations of glaucoma. Emergency Medicine, 14-21.)

Angle of anterior chamber

Angle created by cornea, iris, and trabecular meshwork

Primary glaucoma

Idiopathic increase in IOP

Secondary glaucoma

Increase in IOP from known disease

Open-angle glaucoma

Insidious increase in IOP that can slowly progress to blindness

Acute angle-closure glaucoma

Medical emergency marked by abrupt increase in IOP that can rapidly progress to optic nerve damage and nerve death

A brief note on secondary glaucoma:

  • many secondary causes are rare

    • exfoliative syndrome and pigment dispersion syndrome

      • debris and granules are caught up in the trabecular meshwork and block the flow of the aqueous humor

    • lens-induced glaucoma (lens subluxation or dislocation)

      • structures which drain aqueous humor collapse without the lens support

    • ocular inflammatory disease (can occur with herpes zoster ophthalmicus)

    • intraocular tumors

    • ** topical or systemic corticosteroids

Open-Angle Glaucoma
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