Ординатура / Офтальмология / Английские материалы / Visual Fields Examination and Interpretation_Walsh_2011
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D E
Figure 7-9. (Continued)
fields.6 Treatment with immunosuppressive medication can limit the visual field loss and reduce the risk of developing cystoid macular edema.
7-6 TOXICITY
Hydroxychloroquine (Plaquenil) toxicity may present with pigmentary changes or a bull’s-eye maculopathy on fundoscopic examination associated with a paracentral scotoma. While no gold standard for screening for hydrochloroquine toxicity exists, a standard panel of screening tools includes color vision testing, Amsler grid monitoring, fundoscopy, and Humphrey Visual Field Analyzer 10-2. Fluorescein angiography can help distinguish suspected cases of toxicity. Development of central or paracentral scotomas on Humphrey Visual Field Analyzer 10-2 is highly suspicious for hydroxychloroquine-related maculopathy, even if disruption of RPE is not detected on ophthalmoscopy or fluorescein angiography. Because the scotomata are irreversible, there is often a low threshold to discontinue the medication. The usual recommendation is that patients with normal renal function take no more than 6.5 mg/kg/day, although the incidence of retinopathy at lower doses still exists. As a result, annual screening is very important to detect subtle changes. Other modalities that are being investigated include multifocal ERG testing, high-resolution optical coherence tomography (OCT), and preferential hyperacuity perimetry (PHP).
7-7 PERIPHERAL RETINA
Peripheral retinal abnormalities can also cause visual field changes. Retinal detachments will have relative field defects that correlate with the area of
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Figure 7-10. Oculocutaneous albinism. (A) HVF 24-2, both eyes. Visual field depression particularly prominent in peripapillary distribution. (B) and (C) Fundus photo, right and left eye, with areas of hypoplasia, notably in the peripapillary area. Note central hemorrhage in right eye.
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B C
Figure 7-10 (Continued)
detachment. This is in contrast to retinoschisis, which cause an absolute field defect (Figure 7-13). Peripheral tumors such as ocular melanoma can cause peripheral visual field changes.
Cancer-associated retinopathy (CAR) can cause retinal dysfunction and loss of peripheral and central vision without pigmentary changes. CAR is associated with a rapidly progressive loss of peripheral and central vision. Initial fundus findings can be minimal, often with arterial narrowing. ERG can show severe reduction of rod and cone responses. Eye symptoms can precede the diagnosis of the primary tumor and is often associated with small cell lung carcinoma. Melanoma-associated retinopathy (MAR) has a similar presentation of nonspecific visual field changes
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Figure 7-11. Cone dystrophy. (A) Fundus photo, right eye. Fundus findings can include a subtle bull’s eye maculopathy. (B) HVF 24-2, right eye. Cone dystrophy often presents with central visual field changes.
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Figure 7-11. (Continued)
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Figure 7-12. Ocular histoplasmosis (A) HVF 24-2, right eye, with nasal depression. (B) Ocular. Fundus photo, right eye. There is a central scar and peripapillary changes.
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B
Figure 7-12 (Continued)
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Figure 7-13. Retinoschisis. (A) Goldmann visual field, with superior depression. (B) Fundus photo montage, left eye, with corresponding inferior retinoschisis.
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B
Figure 7-13. (Continued)
that is specifically associated with malignant melanoma. Unlike CAR, MAR is often found in patients who have already been diagnosed with melanoma. In MAR, ERG findings can show a preserved a wave with loss of b waves. Both CAR and MAR are associated with antiretinal antibodies.
REFERENCES
1.Kaiser-Kupfer MI, Caruso RC, et al. Use of an arginine-restricted diet to slow progression of visual loss in patients with gyrate atrophy. Arch Ophthalmol. 2004;122:982–984.
2.Hoffman MB, Seufert PS, Schmidtborn LC. Perceptual relevance of abnormal visual field representations: static visual field perimetry in human albinism. Br J Ophthalmol. 2007;91:509–513.
3.Reddy CV, Brown J Jr, Folk JC, et al. Enlarged blind spots in chorioretinal inflammatory disorders. Ophthalmology. 1996;103:606–617.
4.Gross NE, Yannuzzi LA, Freund KB, et al. Multiple evanescent white dot syndrome. Arch Ophthalmol. 2006;124:493–500.
5.Fine HF, Spaide RF, Ryan EH Jr, et al. Acute zonal occult outer retinopathy in patients with multiple evanescent white dot syndrome. Arch Ophthalmol. 2009;127:66–70.
6.Thorne JE, Jabs DA, Kedhar SR, et al. Loss of visual field among patients with birdshot chorioretinopathy. Am J Ophthalmol. 2008;145:23–28.
8
Optic Chiasm Field Defects
CHRISTINE E. LIN
AND JEFFREY G. ODEL, MD
8-1 HISTORY AND OVERVIEW
The optic chiasm has been a topic of much interest since the first century A.D., when Galen described the union of the optic nerves as a “shape…very much like the letter chi.”1 In the centuries that followed, many scientists and physicians studied the structural aspects of the optic chiasm, starting with Isaac Newton, who in 1706 first explained that the partial decussation of the optic nerve fibers was necessary for binocular vision.1
Abraham Vater and J.C. Heinicke provided the first clinical evidence of hemidecussation in 1723, when they described cases of transient “halved vision” (homonymous hemianopia), presumably of migrainous origin, and concluded that the optic nerves decussate before uniting into the optic tracts because “without decussation of fibers in these nerves divided vision can in no way be explained.”1 The first diagram of decussating fibers was published in 1750 by “Chevalier” John Taylor, an itinerant eye surgeon, notorious for his charlatan ways and a practice “deeply tainted with the dishonest arts of the quack.”2
In 1824, a century after Vater and Heinicke’s work on hemidecussation, William Wollaston reported experiencing two episodes of half vision in each eye. He concluded that this necessitated hemidecussation of the optic nerves at the chiasm.2
The growing body of knowledge of chiasmal anatomy and visual fields culminated in the work of Harvey Cushing on the diagnostic recognition and surgical management of pituitary tumors. In December 1901, a 16-year-old girl was referred to Cushing by Sir William Osler. She had headaches and loss of vision
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and was short, obese, and sexually underdeveloped, appearing as a child of 12. Cushing missed the possible connection of the patient’s symptoms and appearance to the chiasm and the pituitary. After the young girl developed papilledema, Cushing operated first to decompress one cerebral hemisphere and then the other. When both operations failed to restore her vision, he operated a third time on the cerebellum, but the patient died several days later. At autopsy, a large pituitary cyst was discovered. Around the same time, Alfred Frohlich, a friend of Cushing’s from his research days, reported a similar patient from Vienna. Unlike Cushing, Frohlich made the correct localization, and the syndrome of obesity, retarded sexual development, and pituitary tumor was named after him. Embarrassed before his mentor, William Osler, Cushing then made the pituitary body and its relation to the chiasm, visual fields, and optic atrophy subjects of intense personal interest. He went from missing the diagnosis in 1901 to publishing the seminal work on the topic, The Pituitary Body and Its Disorders, in 1912. He also published a series of papers on visual fields and optic atrophy, several with his ophthalmologic colleague Clifford Walker. Through this work, Cushing contributed substantially to our current understanding of chiasmal lesions and their associated effects on the visual fields of patients.3
Evidence of chiasmal dysfunction alerts the ophthalmologist to an intracranial process causing visual loss, possibly neurologic and endocrine dysfunction, and in some cases, loss of life. Since intracranial mass lesions are the cause of the vast majority of chiasmal visual field defects, variants of bitemporal hemianopia require the ophthalmologist to switch gears and inquire about endocrine, neurologic, and systemic symptoms and to obtain a scan of the chiasm or refer the patient to the appropriate consultant.
8-2 ANATOMY OF THE CHIASM
8-2-1 Gross Anatomy. The optic chiasm (transverse diameter of 10 to 20 mm, anteroposterior width of 4 to 13 mm, thickness of 3 to 5 mm) is located above the sella turcica at an incline between 15° and 45° from the horizontal.4,5 In 79% of people, the optic chiasm is located above the diaphragma sella, the dural covering of the sella turcica (Figure 8-1). The chiasm may also be positioned above the tuberculum sella in a “prefixed” position (Figure 8-2) (12%) or above the dorsum sella in a “postfixed” position (Figure 8-3) (4%).6,7 Depending on the position of the chiasm, a space of approximately 10 mm separates the chiasm from the diaphragma sella; variability in chiasm position partially accounts for the range of visual field defects experienced by patients with upwardly expanding pituitary adenomas.8
Anterior to the chiasm is the chiasmatic cistern. Superiorly, the lamina terminalis extends upward from the chiasm to the anterior commissure. Laterally, the internal carotid arteries emerge from the cavernous sinuses pointed towards the posterior optic nerves and chiasm. Just posterior, the interpeduncular cistern contains the infundibulum descending through the diaphragma sella, the hypothalamus, and the third nerves as they emerge from the basis pedunculi. The third ventricle is also
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A
B
Figure 8-1. Normal chiasm. The prechiasmal space is 8 mm long, and the tuberculum sella is 5 mm long. (A) Sagittal section of normal chiasm above diaphragma sella. (B) Photograph, top view. (Source: A redrawn by permission from Rhoton AL Jr, Harris FS, Renn WH. Microsurgical anatomy of the sellar region and cavernous sinus. In: Glaser JS, ed. Neuro-Ophthalmology Symposium of University of Miami and Bascom Palmer Eye Institute. St. Louis: CV Mosby; 1977:75–105. B reprinted by permission from Bergland RM, Ray BS, Tornack RM. Anatomical variations in the pituitary gland and adjacent structures in 225 human autopsy cases. J Neurosurg. 1968;28:93–99.)
present posteriorly; the proximity to the third ventricle explains the vulnerability of the chiasm to compression or infiltration by lesions within the ventricle or an expanded ventricle.4
The anterior cerebral and anterior communicating arteries of the circle of Willis course above the chiasm, while the posterior communicating arteries, the posterior cerebral arteries, and basilar artery pass below.9 Branches from all of these surrounding vessels supply the optic chiasm both superiorly and inferiorly, and there is often significant collateralization, making chiasmal infarct a rare event (Figure 8-4A). Bergland and Ray theorized that the blood supply to the crossing