Radiation-Induced Optic Neuropathy: Clinical and Imaging Profile of Twelve Patients.

BACKGROUND: Radiation-induced optic neuropathy (RON) is a form of delayed radionecrosis of the anterior visual pathways, which develops within months to years after external cranial irradiation and causes severe and irreversible vision loss. Small series reports have adequately documented its clinical features, but imaging characteristics have been less completely described. METHODS: We accrued cases from the University of Michigan Neuro-Ophthalmology Clinic files and from cases coded as "radiation optic neuropathy" at the University of Michigan Medical Center between 1994 and 2017. All patients had undergone 3D-conformal linear accelerator (photon) external beam radiation. We collected clinical details of vision loss, including the temporal relationship to radiation. A single neuroradiologist (E.A.L.) evaluated all available magnetic resonance imaging (MRI) studies, noting the presence of enhancement, expansion, or volume loss of the optic nerves or chiasm, corresponding T2 signal abnormalities, and the absence of demyelination or confounding compressive lesions. RESULTS: Twelve patients (15 eyes) met inclusion criteria. Vision loss was usually monocular at outset, but both optic nerves were eventually involved in 3 (25%) patients. Although usually sudden in onset, vision loss often declined slowly over many months, frequently to finger counting, or worse without recovery. An afferent pupillary defect was always present at the time of presentation. Most affected optic discs were pale at the time of first visual symptoms, indicating that subclinical optic nerve damage had been present for several weeks. The latency from completion of radiation to onset of vision loss ranged from 7 to 48 months (average: 18 months). In 2 patients, radiation was delivered to the whole brain, rather than being limited to the anterior visual pathway. MRI typically displayed a discrete region of enhancement of the affected prechiasmatic optic nerve, often with expansion and high T2 signal in the enhancing segment. In 3 affected eyes, enhancement was apparent on imaging completed 3-6 weeks before the onset of vision loss. In one patient, segmental prechiasmatic enhancement became evident only on repeat MRI completed 7 months after vision loss. The duration of enhancement among 9 eyes with follow-up MRIs was at least 2 months, but in one case, enhancement was still present on a study performed 17 months after treatment. CONCLUSIONS: This study further delineates the profile of RON. Visual loss is often acute, profound, and monocular but may decline slowly after acute onset and later affect both optic nerves. High-resolution MRI of the optic nerves usually will display enhancement of a discrete segment of the intracranial prechiasmatic optic nerve, often with accompanying expansion and T2 hyperintensity. In some cases, these imaging features may precede vision loss. They may be subtle or appear after vision loss. Enhancement lingers for a wide interval, ranging in this study from 2 to at least 17 months. Recognition of these imaging characteristics assists in confirmation of the diagnosis of RON.

Optic Nerve Avulsion After Finger-Poke Injury.

We present a case of optic nerve avulsion as a result of finger-poke injury to the eye. Spectral domain optical coherence tomography demonstrated a plunging cup indicative of the avulsion, a finding not previously described. Optic nerve avulsion is a form of anterior indirect traumatic optic neuropathy evoked by a sudden severe rotation at the junction of the optic nerve and globe induced, in this case, by penetration of the finger into the nasal orbit.

Obstructive sleep apnea and nonarteritic anterior ischemic optic neuropathy: evidence for an association.

Nonarteritic anterior ischemic optic neuropathy (NAION) is the most prevalent optic nerve disorder among patients over 50 years of age, characterized by sudden onset, painless visual loss, with an accompanying relative afferent pupillary defect and optic disc edema. Although the pathophysiology of NAION has not been fully elucidated, several risk factors have been considered, including advanced age, systemic hypertension, diabetes mellitus, and certain optic disc morphologies. An association between obstructive sleep apnea (OSA) and NAION has also been recognized. One prospective cohort study indicated that the relative risk of OSA among patients with NAION was 4.9; a later retrospective cohort study demonstrated that patients with OSA not treated with continuous positive airway pressure (CPAP) had a 16% increased hazard of developing NAION compared to patients without OSA.The following review will discuss the most recent understanding of the relationship between OSA and NAION, with implications for further research and prevention strategies.