Ординатура / Офтальмология / Английские материалы / Field of Vision A Manual and Atlas of Perimetry_Barton, Benatar_2003

DISCUSSION

Field description: Scotomata adjacent to inferior aspect of blind spot and in nasal field, not respecting the meridian, OD.

Localization: Retina.

Pathology: Central serous retinopathy (choroidopathy).

Amsler grid showed an area of distortion inferotemporal to the blind spot.

The patient’s scotomata bear some resemblance to an arcuate defect, with depression near the horizontal meridian and near the blind spot; however, the presence of defects above the meridian argue against this. The location of these defects correlates with sites of retinal pigmentary epithelial changes, shown on fluorescein angiogram from a earlier attack as hyperfluorescent regions (black arrows), rather than with the more extensive zone of subretinal fluid present at that time (white arrows).

The photostress test measures how long visual acuity takes to recover after the retina is bleached by having the patient look at a bright light (4). It is prolonged in macular disease but not optic neuropathy.

The patient’s story of recurrent attacks with resolution might suggest an optic neuritis, although the number of attacks and their long duration are unusual for this condition. Central serous retinopathy is a condition that is easily confused with optic neuritis, since it also causes central field depressions and color defects, affects mainly young people, and its ophthalmoscopic findings are subtle. It can even prolong latencies on visual evoked potentials. However, there is often no or minimal RAPD, compared with optic neuropathy (5). If suspected, a dilated retinal examination and fluorescein angiogram are helpful. The latter shows small hyperfluorescent defects of the retinal pigmentary epithelium, with slow leakage of fluid subretinally behind the neurosensory detachment. Visual defects tend to disappear as the fluid resolves over several months. However, a few patients have a recurrent or chronic central serous retinopathy, as did this patient. Persistent and more severe focal field defects tend to correlate with sites of retinal pigmentary epithelial changes (6).

The cause of this condition remains a mystery. Laser treatment is indicated in those with prolonged serous detachments and permanent visual loss.

HISTORY AND EXAM

This 52-yr-old man with hypertension and hypercholesterolemia had gradually worsening vision in the right eye over 8–10 days without pain. Visual acuity was 20/40 OD and 20/30 OS. Ishihara color plates were 14/14 OU and there was no RAPD (field A). Fundoscopy OD showed disc edema with peripapillary flame hemorrhages, dilated and

tortuous veins, and scattered peripheral hemorrhages. The rest of the neurologic examination was normal. Extensive investigations for coagulopathy were negative. He then returned 3.5 months later with worsening vision OD. His acuity was now 20/400 OD (field B). The vision and fundus OS were always normal.

DISCUSSION

Field description: Field A: mild generalized depression; field B: cecocentral scotoma with enlargement of the blind spot OD.

Localization: Retina.

Pathology: Central retinal vein occlusion (CRVO), ischemic, with macular edema. Confrontation testing showed no abnormality at the initial examination.

The initial field shows mild changes characteristic of nonischemic CRVO, a diagnosis suggested by painless, progressive visual loss with disc edema, dilated tortuous veins, and flame hemorrhages, as in fundus A here. By the patient’s return, however, fundoscopy (B, this page) showed ischemic exudative changes, more hemorrhage, and macular edema

(arrow), indicating a change to ischemic CRVO. On his second field the blind spot is larger, and now, thanks to the macular edema, he has a definite central scotoma with a marked decline in visual acuity.

A number of mechanisms may underlie CRVO, including external compression of the vein; venous stasis from hypoperfusion due to systemic hypotension or carotid arterial stenosis; and degeneration of the venous endothelium, as in patients with diabetes mellitus. There is no recognized treatment of this disorder other than treatment of any underlying disease to prevent a similar occurrence in the fellow eye. Experimental surgical therapies are being investigated for ischemic forms of CRVO, none with proven efficacy yet.

DISCUSSION

Field description: Temporal wedge defect extending from the blind spot OD. Localization: Retinal nerve fiber layer.

Pathology: Presumed ocular histoplasmosis (POHS).

The defect is a narrow wedge that points straight from the temporal periphery to the blind spot, much as the nerve fiber bundle in this area travels. The other eye’s field was normal.

The patient’s fluorescein angiogram (figure) demonstrates the fundoscopic combination of peripapillary and peripheral chorioretinal atrophic scars typical of POHS, as well as mild raised inferonasal gliotic scar of the optic disc. This condition is highly endemic in the Mississippi and Missouri river basins, as well as central America and many river

basins of South America. The organism Histoplasma capsulatum is a fungus found in soil that generates airborne spores that are inhaled. This can lead to an acute or chronic pulmonary condition, and rarely a serious disseminated form that can involve the central nervous system, with meningitis, encephalitis, or myelitis. Patients with POHS often lack systemic or neurologic symptoms, but chest X-ray or serologic testing may reveal signs of earlier infection (7). Whether the ocular signs are a secondary immunologic event or a primary ocular infection is a matter of debate. Most often POHS is discovered incidentally in an inactive stage and does not require treatment. Choroidal or subretinal neovascularization in the macular region may occur and requires photocoagulation to preserve vision. Acute neuroretinitis or papillitis is rarely seen but responds to steroids (8).

DISCUSSION

Field description: Dense superior paracentral scotoma OS.

Localization: Retina.

Pathology: Posterior staphyloma.

Confrontation testing showed decreased red but normal finger comparison in the superior paracentral field OS.

The defect superficially resembles an arcuate defect, but though large it does not reach the horizontal meridian. It also has a fairly extensive relative enlargement of the blind spot, unusual for arcuate defect unless associated with disc edema. The effect of adding a –2.00 spherical lens shrinks the edges of the scotoma,leaving a small area of absolute loss

(the smaller shaded region). Fundoscopy shows the staphyloma that caused the scotoma, which is also evident on ultrasound as a posterior bulge (arrow) of the globe just lateral to the optic nerve (long arrows) in the left eye (left image), compared with the normal eye (right image).

Staphylomas are congenital bulgings of the uvea into a focally thinned sclera. They can be located around the ciliary body or in the posterior retina, usually in a peripapillary location, as in this case. Posterior staphylomata have associated choroidal atrophy, and the posterior bulge is often associated with myopia. The cause is unknown. The main differential is a coloboma, which is a developmental failure of closure of the optic vesicle. Both are static nonprogressive conditions.

DISCUSSION

Field description: Large inferior arcuate defect OD. Localization: Nerve fiber layer.

Pathology: Old chorioretinitis, presumably from toxoplasmosis. Confrontation fields showed an inferonasal step OD to hand motion.

The patient’s arcuate defect looks much like any number of arcuate defects from glaucoma or other optic neuropathies shown later in this atlas (see Case 23). The resemblance is not coincidental. Fundoscopy showed a focal retinal lesion in the superior peripapillary region, which presumably has disrupted the nerve fiber bundle arching in from the temporal retina. These retinal ganglion cell axons are in the innermost layer of the retina and

can be vulnerable to certain retinal diseases as well as optic neuropathy. Such retinal lesions are usually visible on fundoscopy.

Toxoplasmosis is a common cause of chorioretinitis, caused by an obligate intracellular parasite carried by cats and transmitted to humans. Acute lesions are yellowish and associated with a marked vitritis, creating a hazy fundoscopic view. Serologic tests are available and treatment is with sulfadiazine and pyrimethamine. Old healed lesions typically have a highly pigmented chorioretinal scar, as seen here. Congenital toxoplasmosis, spread from the mother to the fetus, can cause cerebral and ocular complications; in the eye the congenital form tends to affect the macula (9).

HISTORY AND EXAM

This 54-yr-old woman noted inferior nasal blurring in the left eye. This had begun to improve by the time she presented a month later. She had no headache, eye pain, or systemic symptoms. Visual acuity was 20/15 OU and color vision was normal. There was no

RAPD. There was slight blurring of the nasal disc OS with a peripapillary flame hemorrhage and a cotton wool spot (soft exudate) at the superonasal disc margin. The remainder of the examination was normal.