Clinical Pathways in Neuro-ophthalmology : An ... - E-Lib FK UWKS

Table 1–12. Clinical Features of Radiation-Induced Optic Neuropathy (RON)
Acute onset of visual loss, gradual or rapidly progressive course
Unilateral or bilateral ‘‘dimming’’ or ‘‘spotty vision’’; bilateral visual loss in 74%
Variable acuity: 20=25–no light perception (NLP); often 20=200
Variable color deficits
Visual field loss
Painless, progressive loss or constricted fields common
May have altitudinal, central scotoma, junctional, or chiasmal field defects
Monocular or binocular transient visual loss may precede by several weeks
Fundus in RON
Initially no optic nerve edema (or pallid edema); that is, almost always retrobulbar
Rarely anterior but then associated with peripapillary hemorrhages and retinal exudates,
especially with radiation retinopathy following treatment of orbital or intraocular lesions
Later atrophic nerve; may be pale initially, optic atrophy over 4 to 6 weeks
Occasional chiasmal syndrome
Occasionally focal retinal pigment epithelium (RPE) loss (choroidal compromise)
Neuroimaging
Non-enhanced T1- and T2-weighted MRI images normal
Often gadolinium enhancement of optic nerves, chiasm, and even tracts
Enhancement usually resolves in several months at which time visual function usually stabilizes
Onset of visual loss
Latency from radiation to onset of symptoms 1 to 144 months, with median delay 13 months after
cessation of therapy
Majority of cases occur within 3 years of radiation therapy
Occurs after radiation for paranasal sinus and other skull base malignancies, but also for pituitary
adenomas, parasellar meningiomas, craniopharyngiomas, frontal or temporal gliomas, and
intraocular tumors; rarely after radiation for thyroid orbitopathy (mainly in diabetics or patients
with more than 2000–2500 cGy)
Radiation dose
Cumulative radiation dose of 2400–12,500 cGy
75% have received total dose of 5000 or more cGy
May occur with stereotactic radiosurgery (Girkin, 1997) if dosage to visual apparatus greater than
8 Gy, large tumor volume, prior visual dysfunction, prior radiation exposure, or treatment
isocenter within 5 mm of anterior visual pathway
Increased risk of RON
Concomitant chemotherapy
Patient with hormone secreting pituitary adenoma
Increased age
Increased risk with increased radiation exposure to optic nerve
Treatment
Unproven treatments
Hyperbaric oxygen (HBO) if started early
Corticosteroids
Others (anticoagulation, antiplatelet agents)
Prognosis
Usually poor visual prognosis
No light perception in 45%
Worse than 20=200 in additional 40%
85% have final visual acuity of 20=200 or worse
Source: Arnold, 1995; Barbosa, 1999; Borruat, 1993, 1996; Ebner, 1995; Girkin, 1997; Glantz, 1994; Goldsmith, 1992;
Gragoudas, 1999; Guy, 1991, 1995; Hudgins, 1992; Jiang, 1994; Landau, 1996; Leber, 1998; Liu, 1992b; McClellan,
1995; Mohamed, 2000; Parsons, 1994; Polak, 1995; Roden, 1990; Tachibana, 1990; Wijers, 1999; Toung, 1992;
Zimmerman, 1990.
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