50  OPHTHALMOLOGY SECRETS IN COLOR

A B

Figure 5-17.  A, Color fundus photography and B, fundus autofluorescence demonstrating a central area of hypoautofluorescence with a surrounding border of hyperautofluorescence in a patient with a presumed hereditary macular dystrophy of unknown etiology (other eye with similar findings).

KEY POINTS: SUMMARY OF KEY MODALITIES FOR RETINAL IMAGING

1. Optical coherence tomography: provides high-resolution cross-sectional images of the retina, retinal pigment epithelium, and choroid and is vital for management of many retinal disorders

2. Fluorescein angiography: provides an assessment of the retinal vasculature using an intravenous dye and is the gold standard for evaluating for the presence of neovascularization in conditions such as diabetic retinopathy, vein occlusion, and age-related macular degeneration

3. Indocyanine green angiography: provides the best assessment of the choroidal vasculature and is helpful in evaluating diseases of the choroid including central serous chorioretinopathy and polypoidal choroidal vasculopathy

4. Fundus autofluorescence: allows for an assessment of the health of the RPE by imaging the intrinsic autofluorescence of the retina

References

1.Galuzzi P, Hadjistilianou T, Cerase A, De Francesco S, Toti P, Venturi C: Is CT still useful in the study protocol of retinoblastoma? AJNR Am J Neuroradiol 30:1760–1765, 2009.

2.Staurenghi G, Sadda S, Chakravarthy U, Spaide RF, International Nomenclature for Optical Coherence Tomography P: Proposed lexicon for anatomic landmarks in normal posterior segment spectral-domain optical coherence tomography: the IN*OCT consensus, Ophthalmology, April 19, 2014.

3.Wong IY, Koizumi H, Lai WW: Enhanced depth imaging optical coherence tomography, Ophthalmic Surg Lasers Imaging 42(4):S75–S84, July 1, 2011.

4.Yannuzzi LA: Indocyanine green angiography: a perspective on use in the clinical setting, Am J Ophthalmol 151(5):745– 751, 2011.

Bibliography

Berson EL: Retinitis pigmentosa and allied diseases: applications of electroretinographic testing, Int Ophthalmol 4:7–22, 1981.

Bilyk JR, Sergott RC, Savino PJ: Quick reference guide for CT and MRI of the eye and orbit, Wills Ophthalmology Review Course, 2012.

Carr RE, Siegel IM: Electrodiagnostic testing of the visual system: a clinical guide, Philadelphia, 1990, F.A. Davis.

De Potter P, Flanders AE, Shields JA, et al.: The role of fat-suppression technique and gadopentetate dimeglumine in magnetic resonance imaging evaluation of intraocular tumors and simulating lesions, Arch Ophthalmol 112:340–348, 1994.

De Potter P, Shields JA, Shields CL: Computed tomography and magnetic resonance imaging of intraocular lesions, Ophthalmol Clin North Am 7:333–346, 1994.

De Potter P, Shields JA, Shields CL: MRI of the eye and orbit, Philadelphia, 1995, J.B. Lippincott.

De Potter P, Shields CL, Shields JA, Flanders AE: The role of magnetic resonance imaging in children with intraocular tumors and simulating lesions, Ophthalmology 103:1774–1783, 1996.

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CHAPTER 5  OPHTHALMIC AND ORBITAL TESTING  51

Deramo VA, Shah GK, Baumal CR, et al.: Ultrasound biomicroscopy as a tool for detecting and localizing occult foreign bodies after ocular trauma, Ophthalmology 106:301–305, 1999.

Fishman GA, Birch DG, Holder GE, Brigell MG: Electrophysiologic testing in disorders of the retina, optic nerve, and visual pathway, ed 2, San Francisco, 2001, American Academy of Ophthalmology. Ophthalmology Monograph.

Marmor MF, Arden GB, Nilsson SEG, Zrenner E: International Standardization Committee: standard for clinical electroretinography, Arch Ophthalmol 107:816–819, 1989.

Newton TH, Bilaniuk LT: Radiology of the eye and orbit, New York, 1990, Raven.

Trope GE, Pavlin CJ, Bau A, et al.: Malignant glaucoma: clinical and ultrasound biomicroscopic features, Ophthalmology 101:1030–1035, 1994.

1.What are the main types of visual-field tests?

•Confrontation visual fields

•Kinetic perimetry

•Static perimetry

•Amsler grids

2.How are confrontation fields used in practice?

Confrontation fields are used as a screening tool because they are a simple, quick, qualitative method for finding gross defects in the peripheral field. The test is performed with the examiner facing the patient and asking if the patient can see fingers in all four quadrants while looking directly at the examiner, testing one eye at a time. In clinical practice, this is more of a screening test. A defect picked up by confrontation fields can be described more definitively with formal field testing.

3.What is the normal field of vision?

From the fixation point, the visual field is 60 degrees nasally, 110 degrees temporally, 75 degrees inferiorly, and 60 degrees superiorly.

4.What is the difference between kinetic and static perimetry?

With kinetic perimetry, a stimulus of a particular size and intensity is moved throughout the visual field. The area within which a given target is perceived is known as that target’s isopter. These are marked with different colors to easily differentiate the multiple stimuli used. Central vision is mapped with dimmer, smaller stimuli. Larger, more intense stimuli are used for peripheral vision. The Goldmann perimeter and tangent screen are examples of kinetic techniques. With static perimetry, a test site is chosen and the stimulus intensity or size is changed until it is large enough or bright enough for the patient to see it. The Humphrey and Octopus machines are examples of static perimetry.

5.When is kinetic perimetry used?

The test can be helpful in patients who require significant supervision to complete visual-field testing, i.e., children, stroke victims, and patients with dementia and other mental challenges. Patients with low vision due to central vision loss are another indication.

Highly trained personnel are needed to administer these tests.

6.What is full-threshold testing?

Full-threshold testing refers to static visual-field testing in which the exact threshold of the eye is measured at every point tested. This technique differs from suprathreshold testing in which test objects are presented at a fixed intensity. Suprathreshold testing is used mainly in screening programs and may miss early defects. Also, a shallow defect will appear the same as an extremely deep defect.

7.You order a Goldmann visual field, and the isopters are labeled with notations such as I2e and V4e. What do these notations mean?

The target size and intensity are indicated by a Roman numeral (I to V), an Arabic numeral (1 to 4), and a lowercase letter (a to e). The Roman numeral represents the size of the target in square millimeters. Each successive number is an increase by a factor of 4. The Arabic numeral represents the relative intensity of the light presented. Each successive number is 3.15 times brighter than the previous one. The lowercase letter indicates a minor filter. The “a” is the darkest, and each progressive letter is an increase of 0.1 log unit.

8.How is an Amsler grid used to test visual field?

The grids can be used to detect central and paracentral scotomas. If held at one-third of a meter, each square subtends 1 degree of visual field.

9.Where is the physiologic blind spot located?

It is in the temporal visual field. The fovea is the center of the visual field. The blind spot is 15 degrees temporal and just below the horizontal plane. On the Humphrey visual field, it is marked by a triangle.

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CHAPTER 6  VISUAL FIELDS  53

10.When looking at a visual field, how do you differentiate the right eye from the left eye?

The right and left eyes are differentiated by noting where the blind spot is located. The right eye has the blind spot on the right side in its temporal field, and the left eye has the blind spot on the left in its temporal field. If the field loss is so great that the blind spot cannot be identified, the top of the printout should say which eye was tested.

11.What are causes of fixation errors? What can be done to decrease them?

•Poor patient fixation

•“Trigger-happy” patient

•Mistake in locating the blind spot

Try replotting the blind spot, reinstructing the patient, or changing the fixation diamond to one that does not require central vision in patients with macular disease or central scotoma. If the fixation loss is greater than 20%, the test is not reliable. Small defects may be missed and the depth of large defects can be underestimated. A kinetic field may be more helpful clinically.

12.What are false-negative errors?

False negatives occur when a stimulus brighter than threshold is presented in an area where sensitivity has already been determined and the patient does not respond. The patient is usually inattentive and the field will appear worse than it actually is. They may also occur in patients with extremely dense defects.

13.What are false-positive errors?

Most projection perimeters are fairly noisy, and there is an audible click or whirring while the machine moves from one position to another in the field. False positives occur when the projector moves as if to present a stimulus but does not and the patient responds. The patient is “trigger-happy,” and the field will look better than it actually is.

14.On a Humphrey visual field, what is the difference between total deviation and pattern deviation?

The total deviation is the point-by-point difference from expected values for normal patients that are in the same age range. It cannot confirm a scotoma, but shows only generalized depression. The pattern deviation adjusts for the generalized depression or elevation and confirms the presence of a scotoma.

15.What is a scotoma?

A scotoma is an area of lost or depressed vision within the visual field surrounded by an area of less depressed or normal visual field. On the pattern deviation plot, three or more nonedge points, clustered in an arcuate area, are suspicious for a scotoma.

16.On a Humphrey printout, what do MD, PSD, SF, and CPSD mean? Are they important?

Mean deviation (MD) is similar to the total deviation plot, i.e., generalized depression. Pattern standard deviation (PSD) is a measure of the degree to which the numbers are different from each other, i.e., local irregularity. This shows more information regarding potential scotomas. Short-term fluctuation (SF) is a measure of intratest error in determining thresholds. Ten predetermined points are each tested twice. Corrected pattern standard deviation (CPSD) is the PSD corrected for the SF. If the SF shows unreliability, the CPSD is better. If the SF is due to true pathology, the PSD is better. If the CPSD or PSD is depressed with p < 5%, it is likely the patient has scotoma.

17.What are false field defects? What are some of their causes?

False field defects occur when the interpreter overlooks physical factors and interprets them as true field defects:

•Ptosis and dermatochalasis can cause loss in the upper parts of the field. Taping the lid up will clear these defects.

•A tilted optic disc can cause local variations in retinal topography, giving the impression of a field defect for refractive reasons alone. When a patient has bilateral tilted discs, the effect can mimic a bitemporal visual field loss.

•A small pupil may give a false impression of true field loss. Dilation of the pupil will clear these defects. This is especially important in patients on miotic therapy (Fig. 6-1).

•The rim of the trial lens will give a defect in the periphery of the central visual field. This will be noted if the patient pulls the head back from the machine while taking the test (Fig. 6-2).

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•Media opacities: cornea, lens, and vitreous opacities may cause routine test objects to be invisible. Using larger, brighter test objects may help clarify this problem. This generalized decreased sensitivity can be noted on the total deviation on a Humphrey visual field, but the pattern deviation may show no defects.

Figure 6-1.  A small pupil can create a false impression of visual-field defects. Note that a majority of the defects disappear or lessen when the pupil is dilated from 2 to 8 mm. (From Gross R: Clinical glaucoma management, Philadelphia, 2001, W.B. Saunders.)

CHAPTER 6  VISUAL FIELDS  55

KEY POINTS: CAUSES OF FALSE-POSITIVE FIELD DEFECTS

1.Ptosis

2.Tilted optic disc

3.Small pupil

4.Rim defect

5.Media opacities

18.What is hemianopia?

Hemianopia is defective vision or blindness in half of the visual field of one or both eyes.

19.Define the terms homonymous and congruous in relation to visual-field defects.

•Homonymous: Pertaining to the corresponding vertical halves of the visual field of both eyes. In plain language, the term is used for defects that occur after neurologic insults that cause loss of a portion of the visual field subsumed by both eyes.

•Congruous: Matched visual-field defects. The more congruous the defect, the more posterior the lesion.

20.How do you describe a visual-field defect?

1.Position: Central (defined as the central 30 degrees), peripheral, or a combination of both. Note if the defects are unilateral or bilateral.

2.Shape: Very helpful diagnostically. Visual-field defects can be monocular or binocular. The most common form of monocular sector defect is found in glaucoma. The shape is determined by physiologic interruption of nerve fiber bundles. The typical binocular sector defect is a hemianopia.

3.Intensity: This refers to the depth of the defect.

4.Uniformity: This refers to the depth of the defect throughout the defect.

5.Onset and course: This is determined by serial visual fields.

21.What are the different types of hemianopia?

•Homonymous, total: Loss of temporal field in one eye and nasal field of the other eye. The vertical midline is respected. The fixation point may be included or spared. This defect implies total destruction of the visual pathway beyond the chiasm unilaterally, anywhere from the optic tract to the occipital lobe. A complete homonymous hemianopia is nonlocalizing.

Figure 6-2.  Rim artifact caused by the lens and lens carrier. This is most commonly seen in patients on whom a hyperopic correction is being used. A clue to the presence of a rim artifact is the abrupt change from a fairly normal reading to a sensitivity of 0 dB. (From Alward WLM: Glaucoma: the requisites in ophthalmology, St. Louis, 2000, Mosby.)

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•Homonymous, partial: The most common visual-field defect. It may be caused by injury to postchiasmal pathways. Again, it can result from damage at any point from the optic tract to the occipital lobe (Fig. 6-3).

•Homonymous quadrantanopia: This is a form of partial homonymous hemianopia.

•Bitemporal: May vary from a loss of a small amount of the temporal field to complete temporal hemifield loss. This defect signifies damage in the optic chiasm.

•Binasal: This defect signifies an interruption of the uncrossed fibers in both lateral aspects of the chiasm, both optic nerves, or both retinas.

•Crossed quadrantanopia: A rare defect in which the upper quadrant of one field is lost along with the lower quadrant of the opposite visual field. It can occur as part of the chiasmal compression syndrome in which the chiasm is compressed from beneath against a contiguous arterial structure. This produces pressure simultaneously from above and below.

•Altitudinal: This defect can be unilateral or bilateral. A unilateral defect is prechiasmal such as that found in an ischemic optic neuropathy. Bilateral lesions may be produced by lesions that press the chiasm up, wedging the optic nerve, such as an olfactory groove meningioma (Fig. 6-4).

•Double homonymous hemianopia: A result of lesions of the occipital area. There is a loss of all peripheral vision with a remaining small area of central vision representing the spared macula of both eyes. Most are vascular in origin, but they can result from trauma, anoxia, carbon monoxide poisoning, cardiac arrest, and exsanguination (Fig. 6-5).

•Macula sparing: This is the rule in occipital damage. The central visual acuity can remain normal.

•Macula splitting: Uncommon and difficult to detect because patient will refixate often during the test. This defect occurs with homonymous hemianopia, caused by lesions in the anterior portion of the postchiasmal pathway.

22.Describe the visual pathway.

The first-order neuron is the photoreceptor, a rod or a cone. They synapse with the second-order neurons, the bipolar cells. These synapse with the third-order neurons, the ganglion cells. Axons from these cells cross the retina as the nerve-fiber layer and become the optic nerve. The arrangement of these fibers determines the visual-field defects seen in glaucoma and other optic nerve lesions.

At the chiasm, the temporal fibers are uncrossed, but the nasal fibers cross. The optic tracts begin posterior to the chiasm and connect to the lateral geniculate body on the posterior of the thalamus. Crossed fibers go to laminae 1, 4, and 6. Uncrossed fibers terminate in laminae 2, 3, and 5. The retinal ganglion cell fibers synapse to cells that then connect to the occipital cortex (area 17) via optic radiations in the temporal and parietal lobes.

23.What visual-field defects are characteristically seen in neuro-ophthalmologic disorders?

The pattern of visual-field loss in these patients can often be used to locate very precisely the area of the visual system involved (Fig. 6-6 and Table 6-1).

24.Describe the visual-field defect in Figure 6-7. What are its major causes?

This is a bitemporal hemianopia. Lesions of the chiasm cause bitemporal hemianopia because they damage the crossing nasal nerve fibers. Masses in this area include pituitary tumors, pituitary

apoplexy, meningiomas, aneurysms, infection, craniopharyngiomas, gliomas, and other less common tumors. In addition, the chiasm may be damaged by trauma (typically causing a complete bitemporal hemianopia), demyelinating disease, and inflammatory diseases such as sarcoidosis and, rarely, ischemia.

25.What causes binasal hemianopia?

Most nasal field defects are due to bilateral arcuate scotomas from glaucoma. True binasal hemianopias are rare, but they are never a result of chiasmal compression. They may be due to pressure upon the temporal aspect of the optic nerve and the anterior angle of the chiasm or near the optic canal.

Causes include aneurysm, tumors such as pituitary adenomas, and vascular infarction.

26.Where would you expect the lesion causing a homonymous hemianopia without optic atrophy to be located?

It should be posterior to the lateral geniculate body. Any lesion anterior to the lateral geniculate body would cause the ganglion axon cells to degenerate.

CHAPTER 6  VISUAL FIELDS  57

Figure 6-3.  Bitemporal hemianopia: incongruous noted on both the Goldmann perimeter (above) and the Humphrey perimeter (below). (From Burde RM, Savino PJ, Trobe JD: Clinical decisions in neuro-ophthalmology, ed 2, St. Louis, 1992, Mosby.)

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Figure 6-4.  Bilateral altitudinal hemianopia. (From Harrington DO, Drake MV: The visual fields: text and Atlas of clinical perimetry, ed 6, St. Louis, 1990, Mosby.)

Figure 6-5.  Double homonymous hemianopia. (From Harrington DO, Drake MV: The visual fields: text and Atlas of clinical perimetry, ed 6, St. Louis, 1990, Mosby.)

CHAPTER 6  VISUAL FIELDS  59

Figure 6-6.  Diagram of the visual pathway with sites of nerve fiber damage and corresponding visual fields produced by this damage. A, Optic nerve: blindness on involved side with normal contralateral field. B, Chiasm: bitemporal hemianopia. C, Optic tract: contralateral incongruous homonymous hemianopia. D, Optic nerve–chiasm junction: junctional scotoma. E, Posterior optic tract, external geniculate ganglion, posterior limb of internal capsule: contralateral homonymous hemianopia, complete or incomplete incongruous. F, Optic radiation, anterior loop in temporal lobe: incongruous contralateral homonymous hemianopia or superior quadrantanopia. G, Medial fibers of optic radiation: contralateral incongruous inferior homonymous quadrantanopia. H, Optic radiation in parietal lobe: contralateral homonymous hemianopia, may be mildly incongruous, minimal macular sparing. I, Optic radiation in posterior parietal lobe and occipital lobe: contralateral congruous homonymous hemianopia with macular sparing. J, Midportion of calcarine cortex: contralateral congruous homonymous

hemianopia with wide macular sparing and sparing of contralateral temporal crescent. K, Tip of occipital lobe: contralateral congruous homonymous hemianoptic scotomas. L, Anterior tip of calcarine fissure: contralateral loss of temporal crescent with otherwise normal visual fields. (Adapted from Harrington DO, Drake MV: The visual fields: text and Atlas of clinical perimetry, ed 6, St. Louis, 1990, Mosby.)

Table 6-1.  Summary of Neuro-Ophthalmologic Visual-Field Defects

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Figure 6-7.  Bitemporal hemianopia. (From Harrington DO, Drake MV: The visual fields: text and Atlas of clinical perimetry, ed 6, St. Louis, 1990, Mosby)

27.Does visual acuity help to locate the cause of a visual-field defect?

Patients with isolated retrochiasmatic lesions do not have decreased visual acuity unless the lesions are bilateral; then the visual acuity color plates are abnormal and the patient would have a relative afferent pupillary defect. Also examine the patient for optic disc abnormalities such as pallor, cupping, and drusen.

28.Describe the visual-field defect in Figure 6-8. What causes this?

This is a cecocentral lesion defined as a lesion involving both the blind spot and the macular area (to the 25-degree circle). Four primary causes are typically cited: dominant optic atrophy, Leber’s optic atrophy, toxic/nutritional optic neuropathy (i.e., tobacco, alcohol, lead, multiple medications), and congenital pit of the optic nerve with a serous retinal detachment. Optic neuritis also may cause cecocentral lesions.

29.Describe the visual-field defect in Figure 6-9. Where is the lesion? Are there any coexistent symptoms?

A “pie-in-the-sky” lesion is a homonymous quadrantanopia involving the superior quadrant. The term indicates a lesion in the optic radiations through the temporal lobe, but similar defects can be seen with occipital lobe lesions as well. These patients often have coexistent seizures and visual hallucinations.

30.Describe the visual-field defect in Figure 6-10. Where is the lesion? Are there any coexistent symptoms?

A “pie-on-the-floor” lesion is a homonymous quadrantanopia involving the inferior quadrant. The term indicates a lesion in the parietal lobe. These patients often have coexistent spasticity of conjugate gaze (tonic deviation of eyes opposite to the side of the lesion when attempting the Bell’s phenomenon) and optokinetic asymmetry (diminished or absent response with rotation of optokinetic objects toward the side of the lesion).

31.Describe the visual-field defect seen in Figure 6-11

A junctional scotoma is a unilateral central scotoma associated with a contralateral superior temporal field defect. Thus, in a patient that comes in with poor vision in one eye, it is very important to check the contralateral visual field for superior temporal field loss.

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CHAPTER 6  VISUAL FIELDS  61

Figure 6-8.  Cecocentral scotoma. (From Burde RM, Savino PJ, Trobe JD: Unexplained visual loss. In Burde RM, Savino PJ, Trobe JD [eds]: Clinical decisions in neuro-ophthalmology, ed 3, St. Louis, 2002, Mosby, pp 1–26.)

Figure 6-9.  Congruous right superior homonymous quadrantanopia following left temporal lobectomy for epilepsy. (From Burde RM, Savino PJ, Trobe JD: Clinical decisions in neuro-ophthalmology, ed 3, St. Louis, 2002, Mosby.)

32.What is the anatomic explanation for a junctional scotoma?

Inferonasal retina fibers cross in the chiasm, passing into the contralateral optic nerve (Willebrand’s knee). The contralateral optic nerve is compressed near the chiasm. These patients have decreased visual acuity and a relative afferent visual defect.

33.What is an optic-tract syndrome?

Mass lesions of the optic tract are usually large enough to compromise the optic nerve and chiasm as well. Patients have an incongruous homonymous hemianopia (Fig. 6-12), bilateral optic disc atrophy, often in a “bow-tie” pattern, and a relative afferent defect on the side opposite the lesion (i.e., the eye with temporal field loss).

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Figure 6-10.  Left inferior quadrantanopia in a patient with a right parietal lobe lesion. (From Kline LB, Bajandas FJ: Neuroophthalmology review manual, ed 4, Thorofare, NJ, 1996, Slack.)

Figure 6-11.  Junctional scotoma from a lesion at the left optic nerve and anterior chiasm. (From Kline LB, Bajandas FJ: Neuro-ophthalmology review manual, ed 4, Thorofare, NJ, 1996, Slack.)

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Figure 6-12.  Incongruous left homonymous hemianopia from a right optic-tract lesion. (From Kline LB, Bajandas FJ: Neuro-ophthalmology review manual, ed 4, Thorofare, NJ, 1996, Slack.)

34.What are the most common visual-field findings in glaucoma?

Glaucoma is a disease of loss of retinal ganglion cells with characteristic optic nerve findings. The classic defects are determined by the anatomy of retinal ganglion cells as they travel to the optic nerve. The axons circle around the fovea in an arc. With damage to the nerve bundles, the classic findings include a nasal step, an arcuate defect within 15 degrees of fixation (also known as a Bjerrum defect), or a Siedel scotoma (a comma-shaped extension of the blind spot; Fig. 6-13). The defect obeys the horizontal midline (in contrast to neurologic field defects, which obey the vertical midline). An exam of the optic nerve is helpful in making the diagnosis in less clear cases. Defects in the optic nerve will predict the visual field loss (e.g., a superior notch of the nerve will be manifested by an inferior arcuate field defect). Usually, the central field is retained until a late stage of the disease. When the central field is lost, a small temporal island may remain.

35.When has the visual field of a person with glaucoma progressed?

The answer remains controversial. First, do not base a diagnosis of glaucoma on one field. If the patient has clear optic nerve damage and corresponding visual field defects, one can make the diagnosis, but the baseline field needs to be repeated because patient performance will improve with practice. A first field with significant defects not corresponding to the clinical optic nerve exam may be full on a second attempt. Improved fixation can also cause field defects to appear more clearly. Persons with glaucoma tend to have more variable visual fields than normal subjects; thus, a single visual field showing worsening should be confirmed with a repeat field. One study concluded that to be certain of progression, one needs a minimum of 5 years of annual visual fields. However, use of clinical correlation can help (Fig. 6-14). Ongoing research is trying to improve our ability to determine which patients are progressing. Newer imaging with ocular coherence tomography, Heidelberg retinal tomography, and scanning laser polarimetry can help determine clinical correlation on visual field testing.

36.Describe the visual field in Figure 6-15. What is your differential diagnosis?

This is a ring scotoma. Severe glaucoma, retinitis pigmentosa, panretinal photocoagulation, vitamin A deficiency, and other retinal and/or choroidal diseases affect the peripheral retina selectively. Aphakic patients may have a prominent ring scotoma from lens-induced magnification of the central field. Clinical exam should differentiate the above easily. Functional visual loss from hysteria or malingering may reveal a ring scotoma on visual-field testing. A Goldmann visual field may be helpful in this situation, as spiraling where an isopter of greater luminance overlaps one that is dimmer can rule out organic disease (Fig. 6-16).

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Nasal step of rönne

Temporal NFB defect of radiating nasal fibers

Bjerrum arcuate scotoma

Isolated scotoma with bjerrum’s area

Figure 6-13.  Common visual-field findings in glaucoma. (From Kline LB, Bajandas FJ: Neuro-ophthalmology review manual, ed 4, Thorofare, NJ, 1996, Slack.)

CHAPTER 6  VISUAL FIELDS  65

Figure 6-14.  Progression of visual-field defects over 3 years. (From Kanski JJ: Clinical ophthalmology: a systematic approach, ed 5, New York, 2003, Butterworth-Heinemann.)

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37.What is the differential diagnosis of general depression of the field without localized field defects?

This is a general sign without diagnostic value, but can be an indication of glaucoma, media opacities, small pupils, refractive error, and/or an inexperienced or inattentive patient.

38.What clinical findings might mimic a neurologic defect?

An altitudinal defect can be seen with a hemibranch artery or vein occlusion. Peripapillary atrophy will reveal an enlarged blind spot. A disciform macular scar will show a central scotoma (Fig. 6-17). Retinal detachment will show a correlating visual-field defect, even after it has been repaired.

Figure 6-15.  Ring scotoma. (From Gross R: Clinical glaucoma management, Philadelphia, 2001, W.B. Saunders.)

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Figure 6-16.  Visual fields in a hysterical patient. The left eye shows spiraling. The right eye shows a fatigue field in which a star-shaped interlacing field results from testing opposite ends of the various meridians. (From Harrington DO, Drake MV: The visual fields: text and Atlas of clinical perimetry, ed 6, St. Louis, 1990, Mosby.)

KEY POINTS: USING VISUAL FIELDS TO DETERMINE CAUSE

1. Monocular defects are prechiasmal except that the far temporal visual field is seen only by one eye. Watch this in an anterior occipital infarct, which can produce a monocular temporal defect.

2. Lesions posterior to the chiasm do not cross the vertical meridian by more then 15 degrees.

3. Patients with postchiasmal defects typically have normal visual acuity, normal pupils, and a normal exam of the ocular fundus. Papilledema, however, may be seen in patients with space-occupying lesions.

4. Use clinical correlation to interpret fields.

39.What does the future hold for visual-field testing?

Most visual field testing done today is standard automated perimetry. The three important advances in visual-field testing are faster algorithms that decrease test time, short-wavelength automated perimetry (SWAP), and frequency-doubling perimetry. The new algorithm uses previous patient responses to help choose the testing threshold and thus takes less time. Test times are approximately 5 minutes per eye, as opposed to 15 minutes with the older algorithms. SWAP may detect field loss earlier than traditional white-on-white perimetry. SWAP uses standard static threshold-testing strategies with

a blue test object on a yellow background. Early results indicate that visual-field defects may be detected several years earlier with SWAP than with standard static testing. Finally, frequency-doubling perimetry is in the early stages of development but may be extremely useful as a screening tool in the future.

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Figure 6-17.  Paracentral scotoma. (From Kanski JJ: Clinical ophthalmology: a systematic approach, ed 5, New York, 2003, Butterworth-Heinemann.)