INTRODUCTION: Ischemic optic neuropathy is the most common optic nerve disorder in patients over age 50 and may be categorized as arteritic and non-arteritic. There are approximately 6000 new cases annually. Obstructive sleep apnea has been implicated as a risk factor in the causation of NAION, but it is unclear if the treatment of obstructive sleep apnea can prevent NAION. It also has not yet been elucidated if the risk of obstructive sleep apnea is higher in patients with NAION. We describe the case of a patient whose obstructive sleep apnea was diagnosed after NAION was identified.
CASE PRESENTATION: A 79 year old male was referred to sleep clinic for evaluation of obstructive sleep apnea after being diagnosed with non-arteritic ischemic neuropathy by ophthalmology. He denied excessive daytime sleepiness, but on polysomnogram was found to have an apnea-hypopnea index of 20.58 with a nadir of 87% on pulse oximetry, indicative of moderate obstructive sleep apnea. CPAP titration with a pressure of 16 cm H2O eliminated virtually all of the respiratory disturbances.
DISCUSSIONS: NAION is a disease characterized by sudden, painless, mostly irreversible, and generally nonprogressive visual loss accompanied by nerve fiber bundle field defects, a relative afferent pupillary defect, and optic disc edema. In approximately 70% of patients it is noticed upon awakening, and is described by the sufferer as a unilateral diffuse blurring or cloudiness in the affected eye. There are two major subgroups of risk factors for NAION: conditions and situations associated with hypovolemia or systemic hypotension and diseases associated with atherosclerosis or hypercoagulable states. Therefore, it is not surprising that obstructive sleep apnea (OSA), which can have profound circulatory changes in the microvasculature, and often coexists in patients with vasculopathy has been identified as a risk factor in NAION. In a case control study, evidence of OSA was found via polysomnography in 71% of 17 patients with NAION, compared to 18% of control patients referred for evaluation of possible restless leg syndrome. In another case series, 89% of 27 patients diagnosed with NAION had OSA. Several potential mechanisms for NAION in OSA have been proposed. These include impaired optic nerve head blood flow autoregulation secondary to the repetitive apneas, hypoxemic effects on the optic nerve, hypercapnea-induced increases in intracranial pressure, or apnea-induced blood pressure variations. In addition, imbalances between nitric oxide (a vasodilator) and endothelin (a vasoconstrictor) may play a role. Despite the putative relationship between NAION and OSA, in a prospective review of 108 patients with treatment with continuous positive airway pressure did not prevent the development of NAION in three patients.
CONCLUSION: Our patient was initially non-compliant with prescribed CPAP therapy, but after explanation of the risks of untreated OSA and the relationship to his ocular dysfunction, his compliance improved. Repeat ophthalmologic examination has not demonstrated progression of his disease.Obstructive sleep apnea has been associated with NAION but it unclear if the reverse is true, i.e. if the incidence of obstructive sleep apnea is elevated in patients with NAION. It is also unclear if the treatment of obstructive sleep apnea can prevent NAION. Although there are many questions regarding the association of NAION to OSA, it may be prudent for sleep specialists to ask sleep apnea sufferers if they have experienced any visual problems and for opthamologist to refer patients diagnosed with NAION for a sleep study.
DISCLOSURE: Faisal Uddin, No Financial Disclosure Information; No Product/Research Disclosure Information