Progression of Vitreous Detachment Leading to Exacerbation of Visual Field Loss in Acute Nonarteritic Anterior Ischemic Optic Neuropathy

Nonarteritic ischemic optic neuropathy (NAION) is the most common acute optic neuropathy in adults older than 50 years. It is presumed to result from the hypoperfusion of posterior ciliary arteries, which typically causes acute painless visual loss, optic disc edema, and inferior altitudinal visual field defect. Although the pathogenesis of NAION is not well understood, there is an association with optic disc anatomy, such as small optic disc size, and, possibly, posterior vitreous detachment (PVD).1,2 Hondur et al3 reported that a partial PVD, not complete PVD, is the most common in NAION and that a small optic disc has stronger gravitational tractional force per unit area, which pulls preferentially on the superior optic nerve head, causing a predominance of superior optic edema and inferior visual field loss. We report a case of a 56-year-old Caucasian man with a history of NAION in the left eye 12 years prior and mild obstructive sleep apnea who developed new right eye inferior visual field loss 1 week after a transient ischemic attack (TIA) localizing to the right side of the brain. He was at the end of a usual 5-mile uphill run when he had sudden onset dysarthria, dizziness, and left-sided arm and facial weakness and sensory changes. He presented to the emergency room, but these symptoms resolved completely within 30 minutes. Comprehensive evaluation in the emergency room revealed no evidence of ischemia on brain MRI and a normal head and neck computed tomography angiography. Transesophageal echocardiogram revealed a small patent foramen ovale. The patient was started on statin and low-dose aspirin. Eight days after this TIA event, patient awoke from sleep with new right eye inferior vision loss. Three days after onset of vision loss in the right eye, his neuro-ophthalmic examination revealed visual acuities of 20/20 in the right eye and 20/100 in the left eye, a left relative afferent pupillary defect (from first event), severe right superior optic disc edema, and chronic left optic atrophy—overall consistent with sequential NAION or pseudo-Foster–Kennedy syndrome. Static perimetry revealed right eye inferior peripheral visual field loss (−3.9 dB) and severe generalized visual field loss in the left eye (−25.3 dB). Optical coherence tomography (OCT) imaging revealed severely thickened right eye peripapillary superonasal retinal fiber layer thickness due to optic disc edema (average: 184 µm, superior: 345 µm, nasal: 177 µm) and a partial PVD with vitreous attachment at the superior optic disc, which is unchanged compared with prior imaging (Fig. 1A, B). Comparison with the OCT 6 years prior revealed relatively unchanged partial PVD in the right eye, with the vitreous attached at the superior optic disc but detached just beyond the disc border. Horizontal and vertical scans through the right optic disc revealed new optic nerve head elevation, thickening of the nerve fiber layer, and an altered angle of the vitreous attachment relative to the superior optic disc. One week after initial evaluation, the patient noted increased right eye inferior visual field loss and ophthalmic imaging showed a new complete PVD (Fig. 1C), consistent with a temporal relationship between worsening of vision loss and complete PVD.FIG. 1.: Horizontal and vertical enhanced depth imaging-optical coherence tomography (EDI-OCT) scans of the NAION eye at (A) baseline (before onset), (B) first presentation, and (C) 1 week after.Progression of optic disc edema and vision loss after initial presenting symptoms in NAION are well described and occur in 16.4% at a median of 24 days.4 Visual field worsening is usually attributed to worsening of optic disc edema due to ischemia, but the cause of progression is unknown. In our case, the progression to complete PVD occurred at the same time as worsening of vision, suggesting a relationship between the dynamics of PVD to vision loss. Our case highlights the importance of careful review of EDI-OCT scan to evaluate whether there is an evolution of a partial PVD and whether that may have contributed to vision loss. Studies have reported a relationship between PVD traction and the evolution of NAION. Parsa and Hoyt proposed a compelling explanation for this potential link. They suggest that the dynamic mechanical stretch of the epipapillary membrane over axons is likely to cause injury during vitreous separation. The subsequent glial and axoplasmic leakage and the inflammatory response are likely to weaken the remaining attachment.1 Given small optic disc size is the most common risk factor for NAION, there is no doubt that the optic nerve head structural factors are important. However, the data on the contribution of vitreopapillary traction or detachment are mixed. It has been shown that vitreopapillary traction can cause optic disc elevation. Furthermore, a 2-stage progression of optic disc edema was recently reported in 16.4% of an NAION cohort and was associated with worse visual prognosis.4 Previous studies examining the relationship between PVD and NAION found similar rates of PVD in both NAION and control groups, but Hondur et al emphasized that partial PVD is actually the most common in NAION and that crowded optic discs may have stronger viteropapillary attachment. The combination of gravitational forces with the stronger vitreopapillary and possibly vitreovascular tractional forces may be the reason why superior optic disc edema with inferior visual field loss is the most common presentation of NAION. Our case shows that NAION evolves for weeks, with remodeling of the papillary and peripapillary structures. The dynamic transformation from partial to total PVD can be one explanation for progression in some patients.1,3 Although some studies report no vitreopapillary traction in the NAION cohort,2,5 the concern with these studies is that they include patients with NAION presenting within 2–4 weeks of symptom onset, and it seems that the progression of the PVD and NAION occurs earlier, possibly during the first week of onset. In addition, 1 study lacked another healthy control group, but the status of PVD was relatively symmetrical in the 2 eyes of the same patient. Therefore, the association between PVD and NAION, if any, should be investigated in patients with NAION longitudinally and within 1 week of symptom onset with the use of healthy controls. PVD and associated traction could be a contributing rather than a causative factor in NAION pathogenesis. STATEMENT OF AUTHORSHIP Conception and design: H. Wu, A. Alkhabaz, F. Nadeau, Y. J. Liao; acquisition of data: H. Wu; analysis and interpretation of data: H. Wu, A. Alkhabaz, F. Nadeau, Y. J. Liao; drafting the article: H. Wu, A. Alkhabaz, F. Nadeau, Y. J. Liao; revising the article for intellectual content: H. Wu, A. Alkhabaz, F. Nadeau, Y. J. Liao; final approval of the completed article: H. Wu, A. Alkhabaz, F. Nadeau, Y. J. Liao.