Optic Neuritis

Mono-ocular vision changes, especially in a young female should prompt you to thinking about this condition. Optic neuritis (decreased visual acuity, relative afferent pupillary afferent defect) can easily be mistaken for papilledema (visual acuity and pupillary reflexes are normal). Making the diagnosis can be difficult in that the majority of patients may actually have a normal fundoscopic exam but give a classic history for "retrobulbar neuritis" (vision changes and pain especially with eye movement). The following picture shows papilledema:

Once you diagnose optic neuritis the patient needs to get IV methylprednisolone (1000 mg) for 3 days followed by oral prednisone (1 mg/kg) for additional 11 days (7).

Other causes of unilateral vision changes without an acute history of trauma include:

Retinal detachment:

Most frequently this occurs as a spontaneous event in patients with a predispositon to it, as a consequence of ocular trauma, or after intraocular surgery. After trauma this may occur months later. Patients will complain of a sudden burst of flashing lights or sparks that may be followed by numerous small floaters or spots in the field of vision. As the retina detaches further they may complain with the classic "dark curtain" progressing across the visual field. If extensive enough they may also exhibit a relative afferent pupillary defect.

Macular degeneration (5):

In the elderly, this is a cause of substantial vision loss. The Framingham study found the prevalence of this condition to be 1.2% in 52-64 year old patients and rising to 19.7% in 75-85 year olds (1). Macular degeneration is usually a slowly progressive disease with small decreases in visual acuity. However, it can become an aggressive variant when choroidal neovascularization occurs with subsequent hemorrhages. Patients may describe metamorphopsia (distortion of the shape of objects in view).

Amarois fugax :

Commonly this is a disease of the elderly since it is secondary to the buildup of cholestoral specifically in the arch of the aorta. It typically presents in patients who have had intravascular procedures (i.e. catherization) but it can occur sponatenously. The fundoscopic picture below was froma a 72-year-old man who was admitted to the hospital with delirium, acute renal failure, increasing hypertension, sudden impairment of vision in the left eye, and severe pain in the left foot. Funduscopic examination of the left eye (Panel A) showed a cholesterol embolus, or Hollenhorst plaque (arrow), at the bifurcation of a retinal arteriole and vascular sheathing distal to the occlusion (arrowheads). No other physical findings were present. Distal pulses were palpable, but two toes later turned purple and one required amputation (2).

Central retinal artery (CRAO) or vein occlusion (CRVO):

Occlusion of the central retinal artery causes retinal infarction and profound vision loss. Occlusion of the central retinal vein has a more varied prognosis. Usually painless, in retinal vein occlusion the classic "blood and thunder" fundus may be found. Risk factors for CRVO include hypertension and atherosclerosis. Glaucoma may be a risk factor but this isn't exactly clear (3).

Vitreous hemorrhage:

Bleeding into the vitreous will also reduce vision in relation to the amount and location of opaque blood. Most large vitreous hemorrhages occur after trauma but also in any condition that causes neovascularization (ex. diabetes, retinal vein occlusion). It may also accompany a subarachnoid hemorrhage secondary to an aneurysm. A CLUE: if the red reflex cannot be seen but the lens appears clear, be suspicious.

Acute glaucoma:

Note the ratio of the diameter of the cup to the diameter of the whole disk which is usually about 0.3 but can increase to greater than 0.7 with severe glaucoma (4). Typically during an acute attack the patient will have severe pain radiating from the affected eye. The cornea is usually hazy from edema, the pupil is mid-dilated and fixed, and the eye is hard to the touch and very tender.

Ischemic optic neuritis:

Typically this will occur in an elderly patient over the age of 50 and will present with sudden, painless monocular visual loss. There is usually a relative afferent pupillary defect and there is swelling of the optic disc. It is important to keep this in mind because this is a common manifestation of Giant Cell Arteritis (6).

Migraine:

This can make it difficult to distinguish from acute glaucoma attack initially but hopefully by physical and fundoscopic exam you will be able to distinguish the two.

Hysteria:

Finally by default, after you have ruled out all the above with a careful history, physical examination and fundoscopic examination, think of this.

As an aside, CMV retinitis is usually a late manifestation of patients with AIDS but it may be the presenting feature of the disease. Usually seen on fundoscopic examination are areas of infarction, hemorrhage, perivascular sheathing and retinal opacification. Here is what CMV retinitis looks like:

References:

  1. Leibowitz HM, Krueger DE, Maunder LR, et al. The Framingham Eye Study monograph: an ophthalmological and epidemiological study of cataract, glaucoma, diabetic retinopathy, macular degeneration and visual acuity in a general population of 2631 adults, 1973-75. Surv Ophthalmol 1980;24:Suppl:335-610.
  2. Bradley M. Images in clinical medicine - Spontaneous atheroembolism. N Engl J Med 332(15), April 1995.
  3. Finkelstein D, Clarkson JG. Branch vein occlusion study group: branch and retinal vein occlusions. Focal Points 1987: clinical modules for opthalmologist 1987;5:1-11.
  4. Quigley HA. Medical Progress: Open-angle glaucoma. N Engl J Med 328(15): 1097-1106.
  5. D'Amico DJ. Medical Progress: Diseases of the retina. N Engl J Med 331(2): 95-106.
  6. Newman NJ. Optic neuropathy. Neurology 1996; 46:15-322.
  7. Optic Neuritis Study Group: The clinical profile of optic neuritis. Experience of the Optic Neuritis Treatment Trial. Arch Ophthalmol 1991; 109: 1673-78.

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